Chapter 046. Sodium and Water (Part 5) Hypovolemia: Treatment The therapeutic goals are to restore normovolemia with fluid similar in composition to that lost and to replace ongoing losses. Symptoms and signs, including weight loss, can help estimate the degree of volume contraction and should also be monitored to assess response to treatment. Mild volume contraction can usually be corrected via the oral route. More severe hypovolemia requires intravenous therapy. Isotonic or normal saline (0.9% NaCl or 154 mmol/L Na + ) is the solution of choice in normonatremic and most hyponatremic individuals and should be administered initially in patients with hypotension or shock. Hypernatremia reflects a proportionally greater deficit of water than Na + , and its correction will therefore require a hypotonic solution such as half-normal saline (0.45% NaCl or 77 mmol/L Na + ) or 5% dextrose in water. Patients with significant hemorrhage, anemia, or intravascular volume depletion may require blood transfusion or colloid-containing solutions (albumin, dextran). Hypokalemia may be present initially or may ensue as a result of increased urinary K + excretion; it should be corrected by adding appropriate amounts of KCl to replacement solutions. Hyponatremia Etiology A plasma Na + concentration <135 mmol/L usually reflects a hypotonic state. However, plasma osmolality may be normal or increased in some cases of hyponatremia. Isotonic or slightly hypotonic hyponatremia may complicate transurethral resection of the prostate or bladder because large volumes of isoosmotic (mannitol) or hypoosmotic (sorbitol or glycine) bladder irrigation solution can be absorbed and result in a dilutional hyponatremia. The metabolism of sorbitol and glycine to CO 2 and water may lead to hypotonicity if the accumulated fluid and solutes are not rapidly excreted. Hypertonic hyponatremia is usually due to hyperglycemia or, occasionally, intravenous administration of mannitol. Relative insulin deficiency causes myocytes to become impermeable to glucose. Therefore, during poorly controlled diabetes mellitus, glucose is an effective osmole and draws water from muscle cells, resulting in hyponatremia. Plasma Na + concentration falls by 1.4 mmol/L for every 100 mg/dL rise in the plasma glucose concentration. Most causes of hyponatremia are associated with a low plasma osmolality (Table 46-2). In general, hypotonic hyponatremia is due either to a primary water gain (and secondary Na + loss) or a primary Na + loss (and secondary water gain). In the absence of water intake or hypotonic fluid replacement, hyponatremia is usually associated with hypovolemic shock due to a profound sodium deficit and transcellular water shift. Contraction of the ECF volume stimulates thirst and AVP secretion. The increased water ingestion and impaired renal excretion result in hyponatremia. It is important to note that diuretic-induced hyponatremia is almost always due to thiazide diuretics. Loop diuretics decrease the tonicity of the medullary interstitium and impair maximal urinary concentrating capacity. This limits the ability of AVP to promote water retention. In contrast, thiazide diuretics lead to Na + and K + depletion and AVP-mediated water retention. Hyponatremia can also occur by a process of desalination. This occurs when the urine tonicity (the sum of the concentrations of Na + and K + ) exceeds that of administered intravenous fluids (including isotonic saline). This accounts for some cases of acute postoperative hyponatremia and cerebral salt wasting after neurosurgery. Table 46-2 Causes of Hyponatremia I. Pseudohyponatremia A. Normal plasma osmolality 1. Hyperlipidemia 2. Hyperproteinemia 3. Posttransurethral resection of prostate/bladder tumor B. Increased plasma osmolality 1. Hyperglycemia 2. Mannitol II. Hypoosmolal hyponatremia A. Primary Na + loss (secondary water gain) 1. Integumentary loss: sweating, burns 2. Gastrointestinal loss: vomiting, tube drainage, fistula, obstruction, diarrhea 3. Renal loss: diuretics, osmotic diuresis, hypoaldosteronism, salt- wasting nephropathy, postobstructive diuresis, nonoliguric acute tubular necrosis B. Primary water gain (secondary Na + loss) 1. Primary polydipsia 2. Decreased solute intake (e.g., beer potomania) 3. AVP release due to pain, nausea, drugs 4. Syndrome of inappropriate AVP secretion 5. Glucocorticoid deficiency 6. Hypothyroidism 7. Chronic renal insufficiency C. Primary Na + gain (exceeded by secondary water gain) 1. Heart failure 2. Hepatic cirrhosis 3. Nephrotic syndrome . Chapter 046. Sodium and Water (Part 5) Hypovolemia: Treatment The therapeutic goals are to restore normovolemia with fluid similar in composition to that lost and to replace. shock due to a profound sodium deficit and transcellular water shift. Contraction of the ECF volume stimulates thirst and AVP secretion. The increased water ingestion and impaired renal excretion. hyponatremia is due either to a primary water gain (and secondary Na + loss) or a primary Na + loss (and secondary water gain). In the absence of water intake or hypotonic fluid replacement,