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Sodium and Potassium Disorders

The body fluid compartments have age-related changes in their fluid and electrolyte components. Pre-term, total body water is 80%, up to 12-years-of-age gets down to 60% for total body water. In the younger ages you use higher figures. Recall as well that changes in serum osmolality affect the extracellular fluid space, because fluids behave as if they are equilibrating osmotically across a semipermeable membrane. So if you have hypotonicity with decreased serum sodium you are going to contract the ECF but in effect you are going to expand the ICF as water goes to a place of higher tonicity. Similarly, with hypertonicity, high serum sodiums, you are going to pull fluid into the ECF and you are going to pull them largely from the ICF. So you get an autotransfusion. That will become important later as we talk about pathogeneses of clinical syndromes that occur.

So this is just what I said. Serum glucose is osmotically active. Hyperglycemia draws water from the intercellular fluid and factitiously lowers the serum sodium. And they may very well ask you something that involves that fact, that glucose pulls water out. So a rule of thumb, ROT stands for rule of thumb.

The way that you evaluate hydration, and weíll go back to it, is with the way that the body excretes sodium. The principle is, that if a patient is dry, the kidney will attempt to keep sodium and not excrete it. So if you look at a fractional excretion of sodium, which is defined as the clearance of sodium divided by the clearance of creatinine - and Iím going to give you the formula in just a second - the urinary sodium divided by the plasma sodium, and thatís divided by the urinary creatinine divided by the plasma creatinine times 100. This is the clearance of sodium, this is the clearance of creatinine.

Other clinical principles of dehydration: the signs and symptoms of dehydration are related to depletion of the ECF, the extracellular fluid volume and in particular, to the depletion of plasma volume. So, children with hyponatremic dehydration, low serum sodiums, inappropriately expand the ECF at the expense of the ICF, as well as having an ECF that is depleted because of the basic problem. As a result, underline more symptomatic. I think itís underlined in your syllabus.

What are the physical findings? You probably all know all of these. Tachycardia remember is the earliest and most sensitive sign. Hypotension is a late sign. If you are at hypotension, the patient is already late into their dehydration. The others are, as you know, lethargy, weak distal pulses, etc. I donít need to read them off with you. Slow capillary refill and the use of capillary refill, people use 2-3 seconds.

Iíve given you a list of the different causes. There is a pseudo-hyponatremia that can be caused by hyperproteinemia or hyperlipidemia, and these are caused just by the water being crowded out of the tube that you are sending for the sample. Itís not real hyponatremia. Iatrogenic water loading and osmotic redistribution of water are both causes that we will see in hospital settings.

The criteria for SIADH are listed in your text. Hyponatremia, plasma hypo-osmolality and urine that is not maximally dilute. Very important. These patients are euvolemic . In fact, maybe a little bit hypervolemic so their fractional excretion of sodium is often not low but high, even though they are hyponatremic. So there is continued sodium excretion commensurate with intake in the presence of hyponatremia and fractional excretion of sodium is usually greater than 1%. There is normal renal function.

We will just go through briefly, the treatment principles of euvolemic hyponatremia. If the situation is acute, or if neurologic symptoms are there, treat at a sodium of less than 120 but donít treat unless the patient is symptomatic or unless the sodium is less than 120 and correct acutely only to a range that gets above 120. If you correct too quickly - this could be a Board question if there is a person who is sufficiently evil that wants to put this in - but the problems that you will get with too rapid correction of hyponatremia is a CNS condition called central pontine myelinolysis.

We go to hypernatremic dehydration. It usually results in Ö by the way, there should be a section in there on the actual correction of hyponatremia that again, in the interests of time, we will not cover. Sodium overload; again, usually the principle is that there is a decreased water intake and/or water losses. Anytime there is an underline, either in your syllabus or up here, this is sort of a link and association. Something you want to think about when you hear about the thing we are discussing. For example, hypernatremia; and we are talking about that there is sodium overload but also decreased water intake. So inappropriate IV therapy or inappropriately prepared oral electrolyte solutions or other formulas. We used to hear a lot about boiled skim milk being given to treat dehydration, and that of course was a high solid load.

Symptoms; once you see one you wonít forget it. The children are very much in distress. They have high fever, they have a high pitched cry. They may have convulsions, stupor, paralysis, their skin is doughy, skin turgor is preserved but itís doughy, and in the most severe situations, death. I will say one thing about

Let me say, parenthetically - this will give you a chance to take a break. This is editorial comment. I am allowed one editorial comment in the Board review course. There is evolving discussion about treatment of hyponatremic and isotonic dehydration, to where we used to teach - the old way of teaching - was the first half of therapy in the first eight hours, then you divide the next half of the therapy one-quarter.

How much water do you give in hypertonic dehydration? You use the rule of fours. The free water deficit says that for every increase of one milliequivalent per liter above 145, that indicates a free water deficit of approximately 4 ml/kg of body weight. Therefore, 4 ml/kg of water of body weight will lower the sodium by 1 milliequivalent assuming no ongoing losses. We usually teach to give that fluid as quarter-normal or third-normal saline so that you donít overshoot and do it too quickly, but the rule of fours tells you how much free water over that 48 or 72 hours one needs to give.

Now, we will move from sodium to potassium and we will talk about hyperkalemia. What is the etiology of hyperkalemia? Number one, an ischemic blood draw. If the tourniquet has been left on too long. Hemolysis, and this is particularly seen in heel stick. And number three, which we call true artifactual.

Okay, transcellular K shifts, another cause for hyperkalemia. For every decrease 0.1 unit in pH, there is an increased serum potassium of 0.6. We see increase in potassiums; metabolic acidosis, and that is usually greater than it is in respiratory acidosis. So metabolic acidosis is more likely to give you hyperkalemia.

True potassium excess; potassium supplements, sodium chloride supplements which are potassium chloride. Antibiotics that have high potassiums, like potassium penicillin, and blood. Particularly old stored blood. Endogenous sources of potassium include hemolysis and hematomas. These are the big ones. Also after surgery, tissue breakdown. DIC, necrosis and GI bleed. You can have decreased renal potassium excretion, renal failure, mineralocorticoid deficiency; for example, Addisonís disease, and drugs that give mineralocorticoid deficiency like angiotensin-converting enzyme inhibitors, by captopril and enalapril. They work by blocking ultimately the generation of aldosterone. NSAIDís, non-steroidal antiinflammatories, drive up potassium. Pseudo-mineralocorticoid deficiency, that is renal tubular unresponsiveness to mineralocorticoids, and certain drugs, potassium-sparing diuretics, raise potassium. These are important to know.

Clinical manifestations are usually weakness, as listed in your syllabus, and cardiac rhythm changes. Remember these, star these. These are important. The important ones, peaked T-waves, prolonged PR interval, ST depression, absence of a P-wave, widened QRS and ultimately ventricular fibrillation. Number one, two, three and five are important in terms of Ö if they show you an EKG on a test with a history of hyperkalemia.

Hypokalemia. The etiology; one needs to assess the etiology by the urinary potassium and the blood acid-base status. Again, in the same way, you can have artifactual hypokalemia with extreme leukocytosis but we usually think about extrarenal and renal losses of potassium.