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Electrolyte Disorders Focus on CME at Université de Montréal Practical Approach To Patients With Electrolyte Disorders When dealing with hospitalized patients, electrolyte disorders, such as hypernatremia, hyponatremia, hyperkalemia and hypokalemia, can cause complications and should be guarded against. By André Gougoux, MD, FRCPC lectrolyte disorders are common clinical Stability of the extracellular fluid. Indeed, the E problems, especially in hospitalized patients. ionic composition of the extracellular fluid sur- Since these disorders are accompanied by signifi- rounding our cells must be maintained within cant morbidity and mortality, an appropriate and physiologic limits by the homeostatic mechanisms rapid treatment is mandatory. of the body. For example, it is important to keep plasma sodium concentration around 140 milli- equivalents per litre (mEq/L) and potassium con- centration around 4 mEq/L. Dr. Gougoux is professor of Hypernatremia and hyponatremia. When medicine and physiology, natremia is too far from the normal value, the University of Montreal, Montreal, induced osmotic shift of water across the cell Quebec. His areas of medical membrane markedly changes the cell volume. interest include renal diseases This volume decreases when hypernatremia and and electrolyte disorders. hyperosmolality shift water from the cells to the extracellular compartment. In contrast, cell vol- The Canadian Journal of CME / June 2001 51 Electrolyte Disorders Table 1 Table 2 Clinical Manifestations Etiology of Hypernatremia of Electrolyte Disorders • Decreased water intake • Hypernatremia/hyponatremia -Decreased thirst -Seizures, coma -No water available -Drinking impossible • Hyperkalemia/hypokalemia -Paralysis • Increased urinary excretion of water -Cardiac arrhythmias -Diabetes insipidus (central or nephrogenic) -Osmotic diuresis (glucose, mannitol) ume increases when hyponatremia and hypo- osmolality shift water into cells. These changes in cell volume are especially important in the central Hypernatremia nervous system and produce seizures, coma and Definition. Hypernatremia occurs when plasma various other neurologic signs and symptoms sodium concentration exceeds 145 mEq/L,2 (Table 1).1 reflecting a deficit of water for the amount of sodi- um in the extracellular fluid. Etiology. In most cases, hypernatremia results from a negative water balance when the water Hypernatremia occurs when plasma intake is lower than its urinary excretion. Two cat- sodium concentration exceeds egories are observed according to the volume and 145 mEq/L, reflecting a deficit of water the aspect of the urine: for the amount of sodium in the 1. Water intake is decreased when only a small vol- extracellular fluid. ume of concentrated urine is excreted. This is observed when: thirst is reduced in various neurologic conditions; when water is not available (e.g., in a desert; and when the Hyperkalemia and hypokalemia. The normal patient is unable to drink for a variety of rea- ratio of around 30 of the intracellular (Ki) over the sons) (Table 2). extracellular (Ke) potassium concentration is 2. Urinary excretion of water is increased increased by hypokalemia or decreased by hyper- when a large volume of dilute urine is obtained in kalemia. The resting membrane potential of -90 patients with central (lack of vasopressin) or millivolts becomes more negative when nephrogenic (renal resistance to vasopressin) dia- hypokalemia increases the Ki/Ke ratio and less betes insipidus. Osmotic diuresis is characterized negative when hyperkalemia decreases this ratio. by the increased urinary excretion of osmoles, Because hyperpolarization and hypopolarization such as glucose, when diabetic patients have a modify the excitability of nerve and muscle cells, marked hyperglycemia, or by the increased uri- they induce paralysis and life-threatening cardiac nary excretion of mannitol, an osmotic diuretic. In arrythmias, including cardiac arrest (Table 1). this condition, hypernatremia results from the uri- 52 The Canadian Journal of CME / June 2001 Electrolyte Disorders nary excretion of an approximately half-isotonic saline solution. Table 3 Treatment. The first step is to minimize, if Example of Hypernatremia Treatment present, the large ongoing loss of water. For example, vasopressin must be given in central •Total body water (TBW) = 42 L (60% of body diabetes insipidus or insulin must be given to weight) markedly hyperglycemic patients. • Natremia = 154 mEq/L (10% rise) The next step is to replace the water loss by • Rx: 4 L (10% of TBW) of water or 5% dextrose the ingestion of water, if possible, or by the in water intravenous administration of 5% dextrose in water. In order to calculate the amount of elec- Table 4 trolyte-free water required to correct the hyper- natremia, the volume of the total body water, or Etiology of Hyponatremia 60% of body weight, is utilized. For example, • With marked expansion and edema before any loss of water, a 70-kg patient has 42 -Congestive heart failure Lof body fluids. If his/her plasma sodium con- -Hepatic cirrhosis centration is 154 mEq/L or 10% higher than the -Acute or chronic renal failure normal value of 140 mEq/L, the patient’s water • With slight expansion (no edema): SIADH deficit equals 10% of the volume of 42 L. This •With contraction and sodium loss patient needs, over the next 24 hours, 4 L of -Renal losses: diuretics water by mouth or the same quantity of 5% dex- -Gastrointestinal losses trose in water intravenously (Table 3). Of SIADH = syndrome of inappropriate secretion of antidiuretic course, the water losses expected during this hormone period also must be replaced. When osmotic diuresis induces hypernatrem- ia, however, a half-isotonic saline solution should be administered to correct the loss in the Hyponatremia urine. Finally, if a severe contraction of the Definition. Hyponatremia is present when plasma extracellular fluid volume produces significant sodium concentration is lower than 135 mEq/L, hypotension, a 0.9% sodium chloride solution representing an excess of water for the quantity of must first be rapidly administered to correct, at sodium in the extracellular fluid. least in part, this volume contraction. A chronic hypernatremia cannot be corrected at a rate faster than 0.5 mEq/L/hour to prevent Facing Chronic cerebral edema, intracranial hypertension and herniation of the brain. In acute hypernatremia, Non-Cancer- the intravenous administration of 5% dextrose (or glucose) in water cannot exceed the rate of Related Pain its metabolism (around 300 ml/hour) to avoid a severe hyperglycemia that is unresponsive to - see page 81 insulin.3 The Canadian Journal of CME / June 2001 53 Electrolyte Disorders uretic hormone (SIADH). The absence of clini- Table 5 cally detectable edema reflects a slight expansion Water and Sodium of the extracellular fluid volume, and is found in Balances in Hyponatremia SIADH. The inappropriate release of antidiuretic hormone (ADH) is encountered with: various Etiology Water balance Sodium balance diseases of the central nervous system; malignant tumors, such as the oat cell lung carcinoma; sev- • Marked + + expansion eral drugs; and during the pre- and post-operative periods. For that reason, intravenous hypotonic • SIADH + — fluids should be avoided in post-operative • Contraction — — patients.4 3. Hyponatremia with contraction and sodium loss. Clinical signs of contraction of the extra- Table 6 cellular fluid volume include weakness, dizzi- Treatment of Hyponatremia ness and orthostatic hypotension (postural drop in arterial pressure). Diuretic-induced renal • With marked expansion and edema losses and gastrointestinal losses from vomiting -Reduce the ingestion of sodium or diarrhea are the most frequent causes. chloride and water Treatment. The category of hyponatremia -Diuretics determines the appropriate treatment:5-7 • With slight expansion (no edema): SIADH 1. Hyponatremia with marked expansion and -Reduce the ingestion of water edema. In these patients, both sodium and water -Adequate amounts of sodium chloride balances are markedly increased (Table 5). The •With contraction and sodium loss progressive reduction of these two positive bal- -0.9% NaCl i.v. 100-125 ml/hour ances, therefore, is the aim of therapy. The NaCl = sodium chloride intake of sodium chloride and water should be moderately restricted and their urinary excre- tion increased by loop diuretics (Table 6). Since a reduced effective circulating volume results Etiology. Hyponatremia is the most common in the nonosmotic stimulation of ADH, this electrolyte disorder encountered in clinical prac- hyponatremia may be very difficult to treat.8 tice and usually one of the following three cate- 2. Hyponatremia with slight expansion (no edema) gories can be identified (Table 4): or SIADH. In this condition, ADH-induced 1. Hyponatremia with marked expansion and water retention and volume expansion are edema. The obvious presence of edema indi- accompanied by a renal sodium loss. The under- cates a significant expansion of the extra- lying cause should be corrected if possible (e.g., cellular fluid volume and is observed in con- the surgical removal of a lung carcinoma or the gestive heart failure, hepatic cirrhosis, and stopping of the drug responsible). The simplest acute or chronic renal failure. way to correct hyponatremia is water restriction, 2. Hyponatremia with slight expansion (no edema) if the intake of sodium is adequate. If hypona- or syndrome of inappropriate secretion of antidi- tremia is symptomatic and more severe,
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