U Na is 10. U -Osm 400. BP is 100/60. HR 115. Skin exam is dry. No edema. (compensated cirrhosis)
a. Hypovolumic (different from dehydration): You can give more fluid with RL (130 meq/L) than with NS (154 meq/L). If overcorrection occurs, then give DDAVP. b. Euvolumic: If SIADH: Volume Restriction; Salt and Furosemide (Lasix) c. Hypervolumic: Volume Restriction: AVP antagonist?? d. Pseudo-hyponatremia: Glucose high, Mannitol, TG, Other Proteins etc. 5 Overall Concepts
Clinical Questions : Understanding Mechanisms: Clinical Question 22 yo M patient with Schizophrenia was seen for fall. Was found to have S-Na of 113. S-osm was 240. U-osm is 46. U-Na is 6. Describe the pathophysiology of Hyponatremia in this patient? 1. Low ADH: Hence, U-osm is low. 2. Hyponatremia is due to lack of enough Salt to drive out the water from body. Hence, it is as low as it can be. This is a perfect example of hyponatremia due to Primary Polydipsia. How would you treat this patient? 1. Fluid restriction. 2. Salt repletion. Ans: While fluid restriction alone with regular diet (that has salt) will work, Salt repletion is the best answer, as that can drive out the water. This is highly affective since ADH is very low. Do not replete a lot of salt, as that will lead to rapid diuresis, and rapid correction of S-Na. He also had hypokalemia when he presented. He was given NS at 75 cc / hr,  At, around 4 am, it was 116. Hence, IV fluid was changed to 1/2NS with K+. Fluid continued at 75 cc / hr. Subsequent changes are as above. At, 730 am it was changed to 1/4 NS with K+. Na, continued to increase. What could have been done upfront to minimize the risk of such a rapid correction of Na. Ans: 1) Instead of 75 c / hr, NS could have been run at 25 cc / hr. That limits amount of Na, and amount of diuresis it can cause, and decreases the rate of correction. 2) At 730 am, since Na continued to go up, instead of changing the 1/4NS with K+, it should have been changed fully to D5, and needed to be given at a rate more than what kidney can handle. i.e @ 250 cc / hr. That would cause hyponatremia, and make sure it reverses. What is the role of S-K+ in hyponatremia, and how does its correction affect S-Na. Further explanation on how hypokalemia causes hyponatremia, and how potassium repletion causes correction of hyponatremia. Hypokalemia is an independent predictive factor for the development of hyponatremia. Because intracellular and extracellular osmolality are always equal, loss of either sodium or potassium, unless accompanied by loss of water, would result in hypotonicity. Although it is intuitively evident why changes in body sodium and water levels should determine serum sodium concentration, the role of potassium is less obvious, but nevertheless is very important. Edelman et al showed that serum sodium concentration is a function not only of total exchangeable sodium and total-body water, but also of total exchangeable potassium. The primary mechanism is that potassium depletion results in a shift of sodium into the cell with a commensurate exit of potassium from the cell into extracellular fluid. The reverse occurs during potassium repletion and explains Laragh’s observation that oral potassium chloride administration resulted in an increase in serum sodium levels in hyponatremic patients in the absence of administered sodium. A similar observation was reported by Fichman et al in patients with diuretic-induced hyponatremia and hypokalemia. This effect of potassium repletion to increase serum sodium concentration may be enhanced by the entry of chloride into cell along with the potassium, which renders the cell hypertonic and draws water from the extracellular fluid. Potassium entry also may be accompanied by the movement of hydrogen ions from the intracellular to extracellular space, where they are buffered and thereby made osmotically inactive. This would decrease effective extracellular tonicity, again causing water to move into the cells, increasing the extracellular concentration of sodium. Whichever mechanism is dominant, the important observation is that potassium depletion could be associated with hyponatremia, and potassium repletion results in an increase in serum sodium concentration. Note: Above paragraph is from the reference included here: http://www.ajkd.org/article/S0272-6386(09)01662-X/abstract Hence, rapid correction of Na in this patient may very well have been partly related to the correction of hypokalemia. Case based discussion 36 yo comes with following.  EKG is as below.  EKG changes of Hypokalemia 1) Depression of the ST segment, 2) Decrease in the amplitude of the T wave, and 3) An increase in the amplitude of U waves which occur at the end of the T wave. U waves are often seen in the lateral precordial leads V4 to V6. 4) Prolongs the QT interval Ref: Up-to-date Patient received 1 L NS bolus in ER. Also, was repeated aggressively with K. Subsequent BMP are as follow.  |
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