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Evaluation of Hyponatremia: a Little Physiology Goes a Long Way

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Evaluation of Hyponatremia: a Little Physiology Goes a Long Way REVIEW BENJAMIN J. FREDA, DO MICHAEL B. DAVIDSON, DO PHILLIP M. HALL, MD Department of Nephrology and Hypertension, Department of Internal Medicine, The Cleveland Staff Consultant, Department of Nephrology and The Cleveland Clinic Foundation Clinic Foundation Hypertension, The Cleveland Clinic Foundation Evaluation of hyponatremia: A little physiology goes a long way ■ ABSTRACT YPONATREMIA (a low plasma sodium con- H centration) is among the most common Hyponatremia is common in hospitalized patients. By laboratory abnormalities that physicians taking a careful and logical approach, one can promptly encounter, yet its causes are among the more recognize the causative factor or factors in nearly all complex in medicine. cases. Most cases of hyponatremia are due to impaired In a study of more than 2,800 hospitalized renal water excretion, and recognizing the cause and patients, 15% had plasma sodium concentra- pathophysiologic process makes it possible to provide tions below the lower end of the reference focused individualized care and avoid mistreatment. range of 134 mmol/L.1 Almost 5% had levels less than 125 mmol/L. ■ KEY POINTS In some instances, hyponatremia repre- sents a true medical emergency, requiring In evaluating hyponatremia, the clinician should immediate intervention to prevent cerebral determine the chronicity or acuity of the hyponatremia, edema. More commonly, hyponatremia may confirm that the patient has true plasma hypo-osmolality, reflect the severity of a causative underlying determine the extracellular fluid volume status, assess illness and be a marker of morbidity and mor- laboratory tests and urine sodium values, and assess any tality. For example, the plasma sodium con- centration is a powerful predictor of severity of exogenous free water intake. heart failure2 and mortality in hepatic cirrho- sis.3 In heart failure and hepatic cirrhosis, effective circulating This paper reviews the pathophysiology blood volume is low, triggering release of antidiuretic and diagnostic evaluation of hyponatremia. hormone and water retention regardless of plasma Armed with a sound understanding of body osmolality. fluid physiology, clinicians should be profi- cient in treating this common disorder and If hyponatremia is severe (plasma sodium < 120 mmol/L), avoid the potentially lethal complications of quickly examine the patient for signs or symptoms of mistreatment. acute neurologic changes (seizures, altered mental status, ■ or focal neurologic signs) that may signal the need for A LITTLE PHYSIOLOGY immediate therapy with hypertonic intravenous saline The plasma sodium concentration is the main and furosemide. determinant of plasma osmolality and there- fore of the total water balance among the Plasma glucose should be measured in all cases of body’s fluid compartments. Perturbations of hyponatremia, and the plasma sodium concentration plasma sodium concentration reflect an under- should be corrected for hyperglycemia. lying disorder involving water homeostasis. The challenge for the physician is to understand the disorder that is causing the hyponatremia. The mechanism, etiology, man- CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 71 • NUMBER 8 AUGUST 2004 639 HYPONATREMIA FREDA AND COLLEAGUES Most body water is within cells lthough the water content of humans one third of the extracellular volume is intravas- A depends on several factors such as age, gen- cular (plasma volume) and two thirds is intersti- der, and amount of adipose tissue, total body water tial. Of the total plasma volume (approximately can be estimated as 60% of body weight in men 4.6 L in a 70-kg man), 85% is in the venous circu- and 50% of body weight in women. Older persons lation and 15% is in the arterial circulation. and those with more adipose tissue have less lean Thus, a 70-kg person has an arterial volume of muscle mass and therefore less overall body water roughly 700 cc.4 As we will discuss, this seemingly than determined from the above estimate. small volume is perhaps the most critical determi- The total body water is divided between the nant of the “fullness” of the body’s circulation that intracellular space (40% of body weight) and is critical to the regulation of the body’s sodium extracellular space (20% of body weight). Roughly and fluid levels. agement, and complications of hyponatremia excreted, this ultrafiltrate must be delivered to are more easily understood if one considers the the diluting segment of the kidney. This physiology of water regulation by the kidney requires an adequate glomerular filtration rate and neuroendocrine axis. and an intact thick ascending limb of the loop of Henle. In the loop of Henle, salt is reab- Hyponatremia is most commonly due sorbed from the ultrafiltrate back into the to decreased renal clearance of water plasma without water. What remains is a rela- Hyponatremia can occur when there is either tively dilute (hypotonic) fluid that proceeds sodium loss or, more commonly, water reten- into the distal nephron. tion. This dilute fluid, made up mostly of water, Movement of water from cells to the will be excreted in the urine if it is not reab- Total body blood can also result in hyponatremia by sorbed in the collecting ducts. The reabsorp- water = 60% of increasing the amount of plasma water rela- tion of water depends on the presence and tive to plasma sodium (see Most body water is activity of ADH. body weight within cells, on this page). (men) or 50% Total body water can increase as a result of ADH secretion is directly tied to osmolality increased intake or decreased renal clearance. In a healthy patient, the ADH level is sensi- (women) Hyponatremia due to increased water intake tive to both the plasma osmolality (deter- happens rarely in patients with normal renal mined primarily by the plasma sodium con- function because one would have to drink centration) and the volume status. more than 20 L/day to overcome the kidneys’ As the volume of plasma water increases, capacity to excrete free water. the sodium concentration decreases, and thus Thus, in almost all cases of hyponatremia, so does the plasma osmolality. This decrease is the problem lies in an impaired ability of the sensed by osmoreceptors in the hypothalamus kidneys to excrete free water due to the action that regulate ADH secretion. These cells are of antidiuretic hormone (ADH, vasopressin). sensitive to changes in plasma osmolality of as ADH plays a central role in most cases of little as 1% above or below normal values, and renal-mediated water retention. ADH activity they respond to decreased osmolality by sig- may be increased appropriately (eg, in hypo- nalling the pituitary to inhibit ADH release. volemia) or inappropriately (eg, in cancer or a In the absence of ADH, normally func- drug effect). tioning kidneys excrete more electrolyte-free water, restoring plasma osmolality and the How the kidneys regulate water balance plasma sodium concentration to normal lev- The fluid that is filtered from the glomerulus els. At a plasma osmolality of less than 275 5 has the same concentration of electrolytes as mOsm/kg H2O, ADH secretion ceases. the plasma. For electrolyte-free water to be Conversely, as osmolality increases, ADH 640 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 71 • NUMBER 8 AUGUST 2004 How heart failure and cirrhosis cause hyponatremia Advanced cirrhosis Heart failure Arterial vasodilation Decreased cardiac output Reduced effective circulating blood volume (decreased tissue perfusion) Physiologic responses Brain Kidney Increased antidiuretic hormone Decreased glomerular filtration release Increased proximal tubular sodium reabsorption Continued water intake Increased proximal tubular water reabsorption Clinical consequences Resultant secondary Increased plasma free water hyperaldosteronism and hyponatremia Sodium avidity and low urine sodium Increased extracellular fluid volume (edema) Inability to excrete free water FIGURE 1 secretion increases. In a normal kidney, this cular tone, which is sensed by carotid and results in the reabsorption of free water and afferent arteriolar baroreceptors. In an Hyponatremia the reduction of osmolality. attempt to restore perfusion pressure to the is usually due tissues of the body, these baroreceptors signal Decreased effective circulating volume: the posterior pituitary to release ADH, result- to impaired Why patients retain water ing in free water reabsorption and hypona- clearance of in heart failure and hepatic cirrhosis tremia, even if the plasma is already dilute.6 In some diseases, the normal mechanisms of The volume of extracellular fluid needed to water water homeostasis go awry, leading the kidney maintain perfusion pressure and avoid stimu- to reabsorb water even though the patient lation of ADH release has been called the appears fluid-overloaded. As a result of water effective circulating blood volume.6 retention, the plasma osmolality decreases, Other mechanisms resulting in water and and hyponatremia ensues. sodium retention in patients with edematous Patients with heart failure or hepatic cir- states are outlined in FIGURE 1. rhosis may continue to retain sodium and Thus, the presence of hyponatremia may water, even though they may have a clinically indicate that underlying heart failure or cir- apparent excess of extracellular fluid volume rhosis is severe enough to limit tissue perfu- (ie, edema or ascites). sion as sensed by the kidney and carotid Diminished cardiac output (in heart fail- baroreceptors. ure) and peripheral vasodilation (in hepatic cirrhosis)
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