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Hyponatremia: Why It Matters, How It Presents, How We Can Manage It

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Hyponatremia: Why It Matters, How It Presents, How We Can Manage It IVOR DOUGLAS, MD, MRCP(UK)* Assistant Professor, Pulmonary and Critical Care Medicine Director, Medical Intensive Care, Denver Health Medical Center University of Colorado at Denver and Health Sciences Center Denver, CO Hyponatremia: Why it matters, how it presents, how we can manage it ■ ABSTRACT YPONATREMIA is common among hospi- H talized patients and can lead to serious Hyponatremia is a common electrolyte disorder among hospi- complications, yet its assessment can be a chal- talized patients and has been associated with increased mor- lenge and strategies for its management have tality. Most patients are asymptomatic, but many do present traditionally been suboptimal. New therapies with symptoms, usually of a generalized neurologic nature. are emerging that promise a more targeted Based on medical history, physical examination (including approach to regulating body water and sodium volume-status assessment), and laboratory tests, patients can balance in patients with this disorder. This be classified as having either hypervolemic, euvolemic, or article reviews the incidence and clinical sig- hypovolemic hyponatremia. Management depends on the nificance of hyponatremia, discusses patient speed of hyponatremia onset; its degree, duration, and symp- evaluation and classification, and surveys cur- toms; and whether there are risk factors for neurologic com- rent and emerging management approaches for plications. The risks of overly rapid correction must be weighed the various types of hyponatremia. against the benefits of treating hyponatremia. Traditional therapies have significant limitations. New agents that ■ DEFINITION AND EPIDEMIOLOGY antagonize arginine vasopressin at the V2 receptor or both the V1A and V2 receptors show promise for treating hyper- Hyponatremia represents an excess of body volemic and euvolemic hyponatremia, as they induce desired water relative to body sodium content and is free water diuresis without inducing sodium excretion. frequently defined as a serum sodium concen- tration of less than 135 mEq/L.1,2 Abnor- ■ KEY POINTS malities of the mechanisms that regulate body Hyponatremia results from changes in total body water, not water and sodium metabolism are often pres- ent in hospitalized patients. Untreated acute body sodium content. These changes are regulated primarily severe hyponatremia is associated with an by thirst, the hormone arginine vasopressin, and the kidney. increase in mortality.3 Hyponatremia is the most common electro- The rate of decline in plasma sodium concentration, the lyte disorder,1 reported to occur in up to 6% of patient’s age, and the extracellular fluid volume affect the hospitalized patients.4 The precise incidence of clinical presentation in patients with hyponatremia. hyponatremia varies depending on the condi- tions underlying it and the criteria used to Prompt, controlled correction of serum sodium is indicated define it.1 When defined as a serum sodium con- for acute symptomatic hyponatremia. Hypertonic saline and centration of less than 135 mEq/L, hyponatremia a loop diuretic are often given to achieve this goal. has been reported in 15% to 22% of hospitalized patients.1 In studies defining it as a concentra- Potentially fatal demyelination can occur with overly rapid tion of 130 mEq/L or less, hyponatremia has serum sodium correction; a moderate rate of correction been described in hospitalized patients at inci- (< 12 mEq/L/day) minimizes this risk. dences of 1% to 4%.1,5 The frequency of hypo- natremia varies by clinical setting as well. In an analysis of the prevalence of hyponatremia * Dr. Douglas reported that he has served as a paid consultant to and is on the speakers’ among 120,137 patients at initial presentation bureau of Astellas Pharma US, Inc. to health care providers, 7.2% of patients in the S4 CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 73 • SUPPLEMENT 3 SEPTEMBER 2006 community-care setting were hyponatremic compared with as many as 28.2% of patients in Algorithm for classifying hyponatremia the acute-care hospital setting.6 Serum sodium <135 mEq/L ■ PHYSIOLOGY OF WATER AND SODIUM BALANCE 280–295 Plasma >295 Hyponatremia is associated with decreased mOsm/kg osmolality mOsm/kg serum osmolality resulting from changes in <280 mOsm/kg 7 Isotonic Hypertonic total body water, not body sodium content. hyponatremia hyponatremia These changes are regulated primarily by Hypotonic hyponatremia thirst, arginine vasopressin (AVP), and the 7 kidney. A net increase in water reabsorption, <100 Urine osmolality >100 however, fails to account entirely for the mOsm/kg mOsm/kg decrease in serum sodium concentration seen 8 in patients with hyponatremia. Excess water intake Impaired renal concentrating ability What stimulates AVP release? Extracellular fluid AVP is synthesized in the hypothalamus and Hypovolemic Hypervolemic transported to the pituitary, where it is hyponatremia hyponatremia stored.7 Changes in effective arterial volume stimulate AVP release, causing a decrease in Urine sodium Urine sodium urine flow, maximal concentration of urine, >20 mEq/L <10 mEq/L >20 mEq/L <10 mEq/L and water reabsorption. The primary stimuli Renal Extrarenal Renal Edematous disorders of AVP release are changes in plasma osmo- solute loss solute loss failure • Heart failure lality and changes in effective arterial volume Urine sodium • Cirrhosis >20 mEq/L • Nephrotic that are sensed by the carotid baroreceptors syndrome and left atrium. Other important stimuli causing AVP release include certain medica- Euvolemic hyponatremia tions (eg, diuretics), pulmonary infections, 7 nausea, and mechanical ventilation. SIADH Reset osmostat Endocrinopathies Potassium depletion • Hypothyroidism • Diuretic use Aging increases likelihood of hyponatremia • Glucocorticoid Several changes in the mechanisms that regu- deficiency late water and sodium balance occur as a nor- SIADH = syndrome of inappropriate antidiuretic hormone secretion mal part of the aging process, such as decreased glomerular filtration rate, decreased renal FIGURE 1. On the basis of volume status, urine osmolality, and urine sodium, blood flow, impaired ability to dilute urine, and patients with hypotonic hyponatremia can be categorized into one of three impaired water excretion.1 These physiologic clinically important classes of hyponatremia: hypovolemic, euvolemic, or changes result in an increased likelihood of hypervolemic. Adapted from references 2 and 10. developing hyponatremia with increasing age. Based on the initial assessment of volume ■ INITIAL PATIENT EVALUATION status, medical history, and laboratory meas- urements of urine osmolality and sodium, The initial evaluation of a patient with patients with hypotonic hyponatremia can known or suspected hyponatremia consists of have their hyponatremia classified into one a careful medical history and physical exami- of three main categories (Figure 1):2,10 nation, including a thorough neurologic • Hypervolemic evaluation and clinical assessment of volume 1 • Euvolemic status. Additionally, laboratory measure- • Hypovolemic. ments of serum electrolytes, glucose, blood urea nitrogen, creatinine, uric acid,1 plasma What to exclude osmolality, urine osmolality,9 and urine sodium Because spurious (normo-osmolar) hypona- concentration may be useful. tremia is a common cause of decreased serum CLEVELAND CLINIC JOURNAL OF MEDICINE VOLUME 73 • SUPPLEMENT 3 SEPTEMBER 2006 S5 HYPONATREMIA OVERVIEW the brain.1 Gastrointestinal symptoms, such Clinical symptoms in severe hyponatremia as nausea and vomiting, are more common in patients with serum sodium levels between 12 Altered sensorium 51.7% 125 and 130 mEq/L. Acute hyponatremia (< 48 hours in duration) in a previously Seizures 22.5% asymptomatic young adult can cause severe central nervous system symptoms even at Nausea/vomiting 4.8% serum sodium levels between 125 and 130 2,13 Gait disturbance/ 3.6% mEq/L. Once the level falls below 125 frequent falls mEq/L, neurologic symptoms predominate.12 Dysarthric speech 2.2% Headache, muscle cramps, reversible ataxia, psychosis, lethargy, restlessness, disorienta- Comatose state 2.2% tion, apathy, anorexia, and agitation are symptoms seen in patients with serum sodium 12 0 10 20 30 40 50 60 levels below 125 mEq/L. Percentage of patients Clinical signs include abnormal sensorium, hypothermia, depressed reflexes, pseudobul- 2 FIGURE 2. Incidences of symptoms observed in a retrospective study of 168 bar palsy, and Cheyne-Stokes respiration. hospitalized patients with severe hyponatremia (serum sodium < 115 mEq/L) in a US medical center. Adapted from data in reference 14. Complications can be severe Complications of severe and rapidly develop- sodium levels, hypertriglyceridemia (> 1,500 ing hyponatremia include seizures, coma, mg/dL) and hyperproteinemia (> 10 g/dL) brainstem herniation, respiratory arrest, per- Accurate should be excluded in patients with compati- manent brain damage, and death. These com- assessment ble clinical syndromes, such as acute pancre- plications result primarily from hyponatremia- induced cerebral edema, which is most often of effective atitis or myeloma, and in patients receiving total parenteral nutrition. seen in patients following surgery or in those arterial volume with primary polydipsia. Menstruating women is key to Clinical presentation are also at elevated risk of severe neurologic complications associated with hyponatremia.11 interpreting Although most hyponatremic patients may appear asymptomatic, severe symptomatic Clinically important hyponatremia
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