Water, Electrolyte, and Acid-Base Metabolism
Jack B. Basil
Devin D. Namaky
DEFINITIONS
Anion gap—The anion gap is the difference between the measured cations and anions in serum, plasma, or urine. For serum, it is estimated by subtracting the sum of the chloride and bicarbonate anions from the sodium cations and is usually expressed in mmol/L or mEq/L:
Bowman space—This is the capsular-shaped space that surrounds the glomerulus at the beginning of the tubular nephron in the kidney. It receives the initial glomerular filtrate.
Effective intravascular volume—This is the proportion of the intravascular volume that is effective in determining the filling pressure of the ventricles and is usually directly related to the central venous pressure. This may not always correlate with the actual intravascular volume.
Extracellular fluid—The body fluid that exists outside of cells. It contains approximately one third of the volume of total body water.
Fractional excretion of sodium—This is the amount of sodium excreted in the urine, expressed as a percentage of the sodium that is filtered by the kidney:
where [Na+]Urine is the concentration of sodium in the urine. [Na+]Serum is the concentration of sodium in the serum, [Cr]Serum is the concentration of creatinine in the serum, and [Cr]Urine is the concentration of creatinine in the urine.
Henderson-Hasselbalch—An equation for calculating the pH of an acid or buffered solution. A modification of this
equation may be used to calculate the pH of blood as follows:
equation may be used to calculate the pH of blood as follows:
where pKa H2CO3 = 6.1, HCO3– = concentration of bicarbonate in the blood, kH CO2 = 0.03 mmol/mm Hg.
Intracellular fluid—The body fluid that exists inside of cells. It contains approximately two thirds of the volume of total body water.
Intravascular volume—This is the same as blood volume and includes intravascular water, as well as plasma, plasma proteins, and other blood products such as red cells.
Metabolic acidosis—Acidosis resulting from increase in acids other than carbonic acid or resulting from the inability of the body to form bicarbonate in the kidney.
Metabolic alkalosis—Alkalosis in which plasma bicarbonate is increased directly, or indirectly as a result of decreased hydrogen ion concentration.
Oncotic pressure—The osmotic pressure exerted by proteins in solution, usually pulling water into the intravascular space. This is also commonly called the colloid osmotic pressure.
Orthostatic hypotension—A decrease in perfusion that is caused by a change from a supine to a standing position. This is generally diagnosed by a decrease in systolic blood pressure of more than 20 mm Hg, or a decrease in diastolic blood pressure of more than 10 mm Hg, and is further suggested by a pulse increase of more than 30 bpm.
Osmotic pressure—The pressure that is needed to prevent water flow between two solutions of different concentrations that are separated by a semipermeable membrane.
Plasma osmolality—The measure of solute per kilogram of plasma. For the purposes of this chapter, this is used interchangeably with plasma osmolarity, which is the measure of solute per liter of plasma. This can be estimated for normal plasma:
Respiratory acidosis—Acidosis secondary to decreased ventilation, usually with a proportionate increase in plasma carbon dioxide.
Respiratory alkalosis—Alkalosis secondary to increased ventilation, usually with a proportionate decrease in plasma carbon dioxide.
Specific gravity—This is the ratio of the density of a substance to the density of water. Under most conditions encountered, this is equal to the apparent specific gravity, which is the ratio of the weight of a substance to the weight of an equal volume of water.
Proper management of fluids and electrolytes in the gynecologic surgical patient is of extreme importance. Gynecologic surgical patients can differ in age, baseline nutritional status, and in the complexity of medical problems that they possess. The stresses of surgery and the bodies’ complex responses to that stress need to be understood to best care for these patients. The tendency to standardize postoperative care for all patients should be avoided.
This chapter focuses on the clinical aspects of water and electrolyte balance, and an understanding of basic renal physiology is a prerequisite.
CLINICAL ASSESSMENT OF DISORDERS OF WATER AND ELECTROLYTE METABOLISM
Disorders of extracellular fluid (ECF) electrolyte composition may be detected by measurement of the serum electrolyte concentrations. Identification of the process (or processes) behind the disturbance of electrolyte composition and the planning of subsequent therapy are critically dependent on the clinician’s ability to accurately assess whether the disturbance in ECF electrolyte composition is associated with volume expansion, volume contraction, or a normal volume.
In the evaluation of a patient’s ECF volume status, it must be kept clearly in mind that the critical volume that is effective in determining cardiac output is the effective intravascular volume (IVV). The most effective IVV is that which maintains an optimal cardiac output and thus maximizes tissue perfusion. Although the actual IVV and the effective IVV are the same in many clinical situations and can be expected to change in direct proportion, in a number of important clinical states, the actual IVV is different from the effective IVV. For example, in acute metabolic acidosis, increased venoconstriction can develop, resulting in an abnormal increase in central venous pressure (CVP) and cardiac output. Under this circumstance, the actual IVV could be less than normal, whereas the effective IVV is greater than normal. Because of the increase in venous tone, an IVV that is lower than normal can maintain a normal effective IVV.
Acute changes in venous tone induced by drugs (e.g., morphine, furosemide, norepinephrine), changes in acid-base status, and the presence of bacterial endotoxin also can disrupt the normal relation between the actual IVV and the effective IVV.
The most reliable clinical means for assessing the status of the effective IVV is the pulmonary capillary wedge pressure. This measurement is an estimate of the pulmonary capillary pressure, which is a measure of the filling pressure of the left ventricle. Factors that increase pulmonary capillary wedge pressure tend to increase cardiac output by increasing capillary outflux. When effective IVV is considered within these constraints, it becomes clear that under virtually any physiologic or pathophysiologic circumstance, an optimal effective IVV is one that results in a pulmonary capillary wedge pressure that is high enough to promote optimal cardiac output but low enough to prevent pulmonary edema.
Fortunately, in most clinical situations, it is not necessary to resort to measuring pulmonary wedge pressure to assess whether a disturbance of ECF composition is associated with an effective IVV that is abnormally high, abnormally low, or normal. Instead, an accurate assessment of the effective IVV usually can be made by a careful clinical assessment using the criteria listed in Table 10.1. This table lists the bedside and laboratory means to assess volume status according to whether the findings are consistent with an effective IVV that is less than normal or an effective IVV that is nearly normal or expanded.
Also shown in Table 10.1 are the conditions under which the given means for evaluating the IVV must be qualified (i.e., the conditions that may render the meaning of the finding indeterminate with respect to the evaluation of IVV). For example, the relation between an increase in weight and a change in IVV is rendered indeterminate if, at the same time, the patient has developed a third space, as in bowel obstruction. In this instance, the entire weight gain could be caused by the accumulation of fluid outside the IVV. Thus, the finding of weight gain in this setting cannot be used as evidence of an increase in effective IVV. Whenever a finding can be significantly qualified,
it should not be used in the assessment of the effective IVV. As many independent means as practical should be used to assess the effective IVV to minimize the effect of possible error on the final decision. The greater the number of independent, unqualified findings that agree in favor of a given clinical decision, the more likely it is that the decision is correct. If such a systematic approach to clinical decision making is used, it should be possible to arrive at an accurate evaluation of volume status in most circumstances.
it should not be used in the assessment of the effective IVV. As many independent means as practical should be used to assess the effective IVV to minimize the effect of possible error on the final decision. The greater the number of independent, unqualified findings that agree in favor of a given clinical decision, the more likely it is that the decision is correct. If such a systematic approach to clinical decision making is used, it should be possible to arrive at an accurate evaluation of volume status in most circumstances.
TABLE 10.1 Assessment of Effective Intravascular Volume | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||
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DATABASE FOR ASSESSMENT OF EFFECTIVE INTRAVASCULAR VOLUME
Body Weight
All patients should be weighed on admission to the hospital and then periodically during their hospital stay. In patients undergoing surgery, or in whom problems in fluid and electrolyte balance are anticipated, weight must be measured daily.
Alterations in body weight are the result of changes in body water content plus solid tissue content (fat, protein, bone). Gains or losses of solid tissue are almost always related to changes in caloric intake and seldom exceed 0.25 kg/24 hours. For example, a patient who takes no calories for 24 hours is forced to consume her endogenous stores of fat and protein to meet the energy requirements for continued life. The complete oxidation of fat yields 9 cal/g, and protein yields 4 cal/g. It can be readily calculated that the complete oxidation of 0.25 kg of solid tissue (in starvation, a mixture of about 87% fat, 13% protein) yields enough calories to meet basal daily energy needs. Thus, changes in weight exceeding 0.25 kg/24 hours are almost always attributable to changes in water balance. Although the relation between body weight and effective IVV can be variable, usually the relation between changes in body weight and IVV can be correctly assessed by the application of the guidelines. The first is that a decrease in body weight below normal (for the patient), and not explained on the basis of inadequate caloric intake, can be assumed
to be accompanied by a decrease in IVV. The second is that an increase in body weight above normal not explained by increased nutrition can be assumed to be accompanied by an increase in IVV except when the weight gain develops in association with the following conditions:
to be accompanied by a decrease in IVV. The second is that an increase in body weight above normal not explained by increased nutrition can be assumed to be accompanied by an increase in IVV except when the weight gain develops in association with the following conditions:
Significant hypoalbuminemia: serum albumin less than 2.5 g/dL
Venous obstruction or congestion
Development of third spaces (e.g., obstructed or ischemic bowel)
Under these three general conditions, an increase in body weight may not reflect an increase in the effective IVV.
Renal Function
Creatinine, a by-product of muscle energy metabolism, is produced at a constant rate that is related to muscle mass. Nearly all of the creatinine produced is excreted by glomerular filtration. Therefore, changes in the concentration of serum creatinine reflect changes in the glomerular filtration rate (GFR), and the clearance of creatinine is an index of the GFR.
Normally, as muscle mass increases, the GFR increases proportionately less. Therefore, on the average, children have lower serum creatinine values than do adults, and large adults have higher serum creatinine levels than do small adults. Because of these considerations, a single range of serum creatinine values cannot be applied to everyone.
The following guidelines are suggested for the evaluation of the IVV in light of the state of renal function. Azotemia can be assumed to result from decreased renal perfusion if the serum creatinine level is elevated, the urine is concentrated (specific gravity higher than 1.015), and renal sodium conservation is present (urine sodium level <20 mEq/L) on a random and untimed urine sample. If the fractional excretion of sodium is below 1%, azotemia can be attributed to decreased IVV, unless the patient has severe liver or cardiac disease causing end-organ hypoperfusion. If severe cardiac failure and severe liver failure (hepatorenal syndrome) can be excluded, the decreased renal perfusion can be assumed to be caused by a decreased effective IVV.
Edema, Ascites, and Pleural Effusion
Effective IVV is increased when edema, pleural effusion, or ascites occurs in the setting of congestive heart failure (CHF). Increased effective IVV cannot be assumed in the presence of edema, ascites, or pleural effusion if there is significant hypoalbuminemia or venous obstruction or if the accumulation of fluid is in a relatively small area of capillary injury (e.g., pleural effusion caused by pulmonary infarction).
Tissue Turgor
Tissue turgor is a function of the elasticity of the solid components of tissue and the degree of distention of the tissues by interstitial fluid. If tissue is depleted of interstitial fluid, it becomes less elastic (i.e., it less readily returns to its original shape after being deformed). Skin turgor is best assessed on the forehead and anterior chest. In patients less than 50 years of age, the turgor of the dorsum of the hand also can be used. In older patients, the elasticity of the solid components of tissue is decreased, and the turgor of the skin becomes unreliable in interpreting changes in interstitial volume.
Central Venous Pressure
The measurement of CVP is a relatively simple but useful means for monitoring cardiac function and cardiovascular status. For the valid measurement of CVP, the catheter must be placed in the large intrathoracic veins near the right atrium (as assessed by chest radiograph), and the catheter must be patent (as assessed by the cyclic variation of CVP with ventilatory movements: decreased CVP during inspiration, increased CVP during expiration).
In normal adults, CVP is about 5 to 12 cm H2O. CVPs below 3 cm H2O are commonly seen in children and young adults who have no evidence of a decreased effective IVV. In older adults and elderly persons, CVP of less than 3 cm H2O can be assumed to reflect a significant decrease in effective IVV.
Central venous pressure is an index of the filling pressure of the right atrium, which, in turn, is an index of the filling pressure of the right ventricle. In uncomplicated circumstances, expansion of the IVV results in increased CVP, whereas contraction of the IVV results in decreased CVP. Central venous pressure cannot be used to assess the adequacy of left ventricular function in patients in whom left ventricular function may be impaired relative to right ventricular function. Central venous pressure also is unreliable when lung disease is present, because it is commonly falsely elevated. In such patients, left ventricular function can be monitored by observing for signs and symptoms of left ventricular failure (dyspnea, development of an audible third heart sound, or pulmonary edema), or by direct measurement of pulmonary capillary wedge pressure. Under normal circumstances, the pulmonary capillary wedge pressure is about equal to the CVP plus 6 mm Hg.
Pulmonary Capillary Wedge Pressure
Technical refinements of the Swan-Ganz catheter make it possible to measure pulmonary artery systolic and diastolic pressure, CVP, pulmonary wedge pressure, and cardiac output using the thermodilution technique with the same catheter. This permits a definitive assessment of the volume status of the patient, because it can be determined whether the cardiac output is appropriate for a given pulmonary wedge pressure. Specific guidelines for the interpretation of the relation between pulmonary wedge pressure and cardiac output are discussed in the following sections.
Patients with Normal Volume Status
Pulmonary wedge pressure can be expected to be between 8 and 12 mm Hg in a patient with a normal cardiopulmonary system and a normal effective IVV. Cardiac output is normal. Pulmonary wedge pressure can be less than 8 mm Hg without indicating volume contraction; in this circumstance, the cardiac output is normal despite the unusually low pulmonary wedge pressure.
Patients Who Are Volume Contracted
Patients who have a normal cardiopulmonary system but who are significantly volume depleted usually have a pulmonary wedge pressure below 8 mm Hg and their cardiac output is less than normal. In patients with chronic pulmonary hypertension (e.g., those with chronic left ventricular failure), a higher than normal pulmonary wedge pressure is needed to drive a satisfactory cardiac output. Thus, in such patients, pulmonary wedge pressure can be above the normal range but be inappropriately low for the patient. This situation can be identified by showing that: (a) cardiac output is less than normal, despite the elevated pulmonary wedge pressure; (b) volume infusion causes an increase in cardiac output toward a more favorable range; and (c) despite further increase in pulmonary wedge pressure with volume expansion, pulmonary function does not deteriorate. (Pao2 does not decrease, PaCO2 does not increase, and pulmonary compliance does not worsen.)
Patients Who Are Volume Expanded
In patients with a normal cardiopulmonary system, pulmonary wedge pressure usually is above 18 mm Hg when volume expansion is substantial. Cardiac output is above normal. If cardiac function is impaired, cardiac output will be inappropriately low for the level of pulmonary wedge pressure.
When a given pulmonary wedge pressure is being interpreted, the serum albumin level also should be taken into consideration, because this opposes the effect of capillary hydrostatic pressure to cause migration of fluid from the capillary lumen to the interstitial space. Thus, at any given elevated pulmonary wedge pressure, pulmonary edema develops more rapidly in a patient who is hypoalbuminemic than in one who has a normal serum albumin concentration. In some patients, it is not possible to obtain a reliable pulmonary wedge pressure. In most of these patients, the pulmonary artery diastolic pressure is a good estimate of the pulmonary wedge pressure. If pulmonary hypertension is present, then pulmonary vascular resistance is increased; thus, pulmonary artery diastolic pressure may not be a good index of the pulmonary wedge pressure. In such patients, it is important to be able to obtain a wedge pressure. Finally, in patients who are being ventilated with high levels of positive end-expiratory pressure, pulmonary wedge pressure may become an unreliable index of left atrial filling pressure because the high intrapulmonary pressures may cause obstruction of the catheter orifice. Patients must be briefly taken off the ventilator for accurate measurements. Other circumstances in which pulmonary artery wedge pressure measurements may be inaccurate include the presence of mitral stenosis or pulmonary venous obstruction.
Blood Pressure
The following guidelines are suggested for the evaluation of the effective IVV from measurement of blood pressure.
1. A nearly normal or expanded effective IVV can be assumed in patients with hypertension that is demonstrated in the sitting or standing position.
2. Effective IVV may be decreased in patients who previously were hypertensive but who have become normotensive.
3. Effective IVV may be decreased in patients who develop orthostatic hypotension (a drop in systolic pressure greater than 10 mm Hg in changing from the supine to the sitting or standing position).
Orthostatic hypotension also can be present, in the absence of volume contraction, as a result of prolonged bed rest, during the use of such antihypertensive agents as methyldopa (Aldomet) or of vasodilators (prazosin, minoxidil). If the pulse rate does not rise as blood pressure falls when a patient stands, autonomic neuropathy should be considered as a cause of postural hypotension.
Systemic Vascular Resistance
Normal values are 50 to 150 dyne-s/cm for pulmonary vascular resistance and 800 to 1,200 dyne-s/cm for systemic vascular resistance. Pulmonary vascular resistance is elevated in hypovolemic shock, cardiogenic shock, pulmonary embolism, or airway obstruction; it is diminished in septic shock. Systemic vascular resistance is elevated in hypovolemic shock, cardiogenic shock, pulmonary embolism, and sometimes in right ventricular infarct and cardiac tamponade; it is decreased in end-stage liver disease and septic shock.
CLINICAL ASSESSMENT OF DISORDERS OF EXTRACELLULAR FLUID COMPOSITION
Hyponatremia
The schema for the evaluation of a hyponatremic patient depends on the assessment of volume status. That is, it must first be determined whether the patient’s hyponatremia is associated with an effective IVV that is decreased, normal, or increased. Once this is decided on the basis of the assessment of IVV, a further separation, based only on the state of renal sodium and water excretion, is made. Each of the final categories contains relatively few diagnostic possibilities, and the presence or absence of each of these conditions in a given patient usually can be readily determined. The scheme for the evaluation of a hypernatremic patient is analogous, except that it depends on the assessment of the state of renal water excretion.
Clinical Assessment
In the discussion that follows, only patients with true hyponatremia are considered (i.e., hyponatremia in which serum osmolality is decreased in proportion to the reduction in serum sodium concentration, after appropriate correction for any elevation in the plasma urea nitrogen). By making this distinction, hyponatremia caused by accumulation of ECF solutes such as glucose or mannitol can be excluded. In this type of hyponatremia, the decreased concentration of ECF sodium is the result of the shift of water from cells to the ECF in response to the osmotic gradient caused by the accumulation of the solute. As a consequence, the hyponatremia is associated with an increased plasma osmolality. These patients also can be readily identified either by the presence of hyperglycemia sufficient to explain the decrease in serum sodium concentration or by a history of administration of large amounts of mannitol (0.100 g in adults), usually in the presence of a decreased capacity to excrete mannitol (decreased GFR).
Also to be excluded are patients with spurious hyponatremia that results from the abnormal accumulation of plasma lipids or proteins. In such circumstances, the concentration of sodium in plasma water is normal; however, the concentration of sodium expressed per liter of whole plasma is reduced because an abnormally large volume of whole plasma is occupied by the lipids or proteins, which do not contain plasma water and electrolytes. Thus, when aliquots of hyperlipemic or hyperproteinemic plasma are analyzed, a lower amount of sodium is determined to be present in a given volume of whole plasma. Plasma osmolality, however, is normal because lipids and proteins do not contribute importantly to plasma osmolality (see section on osmotic forces). Patients with spurious hyponatremia can be readily identified by the presence of markedly elevated total serum protein levels (e.g., multiple myeloma) or grossly lipemic serum. The distinction can be readily made if lipemic serum is subjected to centrifugation and the lipoprotein layer is removed before evaluation, if flame photometry is being used for measurement of serum Na+. Spurious hyponatremia is no longer a consideration in most laboratories, because serum Na+ concentration is determined by ion-specific electrodes, and increased levels are not affected by lipemic serum. Symptoms of hyponatremia include increased tendon reflexes, lethargy, mental confusion, and muscle twitching, which are followed by convulsions, coma, and possibly death if levels fall below 115 mEq/L.
Hyponatremia and Volume Depletion Associated with Renal Sodium Wasting
The normal renal response to volume depletion and hyponatremia is the virtual elimination of sodium from the urine
(Fig. 10.1; see section on sodium balance). Thus, the presence of an excessive amount of urinary sodium under these conditions indicates that renal sodium loss is the cause or a major contributing factor to the state of sodium depletion. A spot urine sodium concentration greater than 40 mEq/L, a %E/FNa above 1%, or a urinary sodium excretion rate greater than intake indicates such renal sodium wasting. The conditions discussed in the following sections are associated with hyponatremia, IVV depletion, and renal sodium wasting.
(Fig. 10.1; see section on sodium balance). Thus, the presence of an excessive amount of urinary sodium under these conditions indicates that renal sodium loss is the cause or a major contributing factor to the state of sodium depletion. A spot urine sodium concentration greater than 40 mEq/L, a %E/FNa above 1%, or a urinary sodium excretion rate greater than intake indicates such renal sodium wasting. The conditions discussed in the following sections are associated with hyponatremia, IVV depletion, and renal sodium wasting.
Chronic Renal Disease
All types of renal disease can be associated with renal salt wasting. In adults with such a disorder, the serum creatinine level is virtually always above 2 mg and usually much higher before a significant salt leak develops. These azotemic patients usually require 85 to 170 mEq of sodium daily (5 to 10 g of sodium chloride) to maintain salt balance at a normal effective IVV. Thus, if sodium intake is decreased in azotemic patients by anorexia or vomiting, or if additional sodium losses occur (e.g., diarrhea or diuretic therapy), the inability of the diseased kidneys to conserve sodium and water normally may rapidly lead to the development of significant sodium and water deficits. Water intake usually continues; therefore, sodium balance is more adversely affected than is water balance. As a consequence, the patient becomes volume contracted with hyponatremia. With the onset of CHF or the nephrotic syndrome, the salt leak of chronic renal failure usually disappears, and salt intake must be restricted.
Diuretic Therapy
The diuretics include thiazide agents or loop diuretics, such as furosemide, bumetanide, and ethacrynic acid. Diuretics induce a renal salt-wasting state, and if the urinary output of sodium exceeds intake, sodium depletion ensues. Rarely, diuretics cause hyponatremia without evidence of volume depletion if severe potassium depletion has resulted from their use (Fig. 10.1).
Adrenal Insufficiency (Addison Disease)
Destruction of the adrenal gland or sudden withdrawal of chronic, daily glucocorticoid therapy results in inadequate adrenal function. The lack of mineralocorticoid causes wasting of renal salt but retention of renal potassium and leads to sodium depletion. The lack of glucocorticoid results in a decreased capacity to excrete a water load and leads to hyponatremia but not to volume depletion or hyperkalemia.
Hyponatremia and Volume Depletion Associated with Renal Sodium Conservation
A spot urine sodium concentration of less than 20 mEq/L or a %E/FNa below 1% in a hyponatremic, volume-contracted patient is evidence of normal renal sodium conservation and indicates that the cause of the sodium depletion is nonrenal in origin or that it occurred during previous diuretic therapy. The fact that the serum sodium concentration is lower than normal indicates that water balance is less negative than is sodium
balance. The conditions discussed in the following sections can result in volume depletion and hyponatremia as a result of extrarenal losses of sodium.
balance. The conditions discussed in the following sections can result in volume depletion and hyponatremia as a result of extrarenal losses of sodium.
 FIGURE 10.1 Approach to the assessment of a hyponatremic patient.This approach considers only patients with true hyponatremia (i.e., in nonazotemic patients, serum osmolality is reduced in proportion to the decrease in serum sodium). Thus, patients are excluded who have lowered concentrations of serum sodium because of hyperlipidemia, hyperproteinemia, or the abnormal accumulations of solutes in the extracellular fluid (ECF), such as glucose or mannitol. ADH, antidiuretic hormone; ECT, extracellular fluid; %E/FNa, fractional excretion of sodium; GI, gastrointestinal; IVV, intravascular volume. |
Gastrointestinal Losses
If losses of fluid from the upper gastrointestinal tract (e.g., vomiting, gastric aspiration) cause the hyponatremia, and if the gastric juice is normally acid, metabolic alkalosis is present. If diarrheal losses cause the hyponatremia, metabolic acidosis may be present. In patients with gastric achlorhydria, upper gastrointestinal losses also can lead to metabolic acidosis.
Losses of Sodium from the Skin
Sweat contains about 50 mEq/L of sodium and is a hypotonic fluid. If sweat losses are not replaced, then hypernatremia can develop. In most situations, the water losses from the skin are replaced more adequately than are the sodium losses. Thus, most patients with significant sodium losses that are due to sweating become hyponatremic. Skin losses of fluid and electrolytes also can occur after burns or other skin injuries. These are isotonic losses of sodium and lead to hyponatremia if the water losses are more adequately replaced than are the sodium losses.
Losses of Sodium from Prior Diuretic Therapy
The natriuretic action of most diuretics lasts less than 24 hours. Hyponatremia is made worse if water intake is excessive.
Hyponatremia and Normal Volume Status Associated with Water Diuresis
In a patient with normal renal function who has become hyponatremic as a result of the administration or ingestion of excessive amounts of water, intravascular and ECF volume are normal to slightly expanded, and high rates of urine flow in association with maximally, or nearly maximally, dilute urine can be expected. In a patient with preexisting renal functional impairment, water loading also increases urine flow rate and dilution of the urine; however, maximally dilute urine cannot be formed. Hyponatremia secondary to water loading may occur in compulsive water drinkers, who usually are severely neurotic or psychotic, or after excessive IV administration of hypotonic fluids. Many of these patients also have high levels of antidiuretic hormone (ADH) for various reasons (e.g., drugs, psychosis). Without this elevation of ADH, presuming normal renal function, consumption of 20 L of water a day would be necessary for development of frank hyponatremia.
Hyponatremia and Normal to Slightly Elevated Volume Status Associated with Water Conservation
As discussed, it is appropriate to observe a brisk water diuresis in a patient with normal renal function who is hyponatremic and has evidence of normal or slightly elevated IVV without edema. When high flow rates of hypotonic urine are not observed, the patient is exhibiting an inappropriate antidiuresis. This may result from the inappropriate release of ADH, although other mechanisms also can be involved (e.g., decreased renal blood flow, certain drugs). Another characteristic of such patients is that administered sodium is promptly excreted in the urine, perhaps because of the effect of atrial natriuretic factors. On the other hand, when sodium intake is curtailed, renal sodium conservation is observed. These patients also exhibit normal adrenal and renal function and are not edematous. The syndrome of inappropriate antidiuresis has been associated with various clinical states, including malignant tumors (e.g., in the lung or pancreas), central nervous system (CNS) disorders (e.g., head trauma, meningitis), infections (e.g., tuberculosis, bacterial pneumonias), the postoperative state, hypopituitarism, and myxedema, as well as with many drugs (Table 10.2). Infusion of oxytocin to induce uterine contraction also can cause hyponatremia because of the antidiuretic effects of oxytocin.
Within the category of hyponatremia associated with normal IVV are three special categories. The feature that sets these apart is that patients may exhibit evidence of water conservation when water is withdrawn or an appropriate or nearly appropriate water diuresis when water is administered. That is, it appears that osmoregulation has been reset to “defend” a lowered plasma osmolality. The first special category includes patients who have an unusual response to diuretic therapy, characterized by hyponatremia, severe potassium depletion, and metabolic alkalosis. Despite the hyponatremia and normal IVV, exchangeable sodium is nearly normal, suggesting intracellular movement of sodium. Magnesium levels should be assessed, and potassium replacement must be accomplished before specific treatment of hyponatremia. The second category involves patients with an unusual manifestation of a chronic illness, such as pulmonary tuberculosis, that resets the osmostat. The third category includes patients with sodium depletion resulting from any cause in whom the decrease in effective IVV is minimized by excessive water intake and retention. This effect of excessive water intake can occur in any of the causes of sodium depletion.
Hyponatremia Associated with Increased Effective Intravascular Volume or Increased Extracellular Fluid Volume (Edema or Ascites)
Congestive Heart Failure
When hyponatremia develops spontaneously in the course of chronic CHF (i.e., is not the result of excessive water administration or diuretic therapy), it usually is indicative of severe cardiac insufficiency and has a poor prognosis. The cause of the hyponatremia in such patients has been ascribed to a decreased capacity to increase renal free water clearance perhaps because of (a) increased fractional reabsorption of glomerular filtrate proximal to the renal diluting sites of the distal nephron and (b) an elevated ADH level.
Cirrhosis of the Liver
Patients with cirrhosis and ascites have a decreased capacity to excrete a water load, possibly because of the same mechanisms at work in patients with CHF.
Excessive Administration of Hypotonic Fluids
This usually is an iatrogenic situation and must be especially guarded against
in postoperative patients whose ADH levels are elevated because of stress, pain, hypovolemia, or drugs, as well as in elderly patients who are unable to maximally dilute their urine.
in postoperative patients whose ADH levels are elevated because of stress, pain, hypovolemia, or drugs, as well as in elderly patients who are unable to maximally dilute their urine.
TABLE 10.2 Antidiuretic Drugs | ||||||||||||||
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Hypernatremia
All patients with hypernatremia are volume contracted, except those in whom the disorder develops as a result of excessive administration of hypertonic saline or sodium bicarbonate and the rare patients with essential hypernatremia (Fig. 10.2). The following discussion considers only the first group of patients; the latter section on treatment discusses all forms of hypernatremia. Patients with hypernatremia usually have CNS deficits, and they may also have confusion and neuroseizures. Autopsy findings often reveal hemorrhages or thromboses of brain tissue.
Hypernatremia Associated with Formation of Concentrated Urine
The normal renal response to decreased intake of water or increased extrarenal losses of water is the formation of maximally concentrated urine. In most clinical situations in which hypernatremia is the result of water depletion, the expected renal response is a Uosm😛osm ratio greater than 1.5 and a specific gravity above 1.015. Thus, the finding of hypernatremia with evidence of renal conservation of water indicates that the hypernatremia is caused by excessive nonrenal losses of water or solute diuresis.
Excessive Nonrenal Water Loss
Hypernatremia typically develops in patients with accelerated rates of nonrenal water loss owing to a hot environment, fever, or hyperventilation, and in whom water losses are not replaced because the patient cannot perceive or communicate thirst. Despite the hypernatremia, sodium deficits usually are present because initially, as water deficits develop, renal sodium excretion increases to maintain normal plasma osmolality and serum sodium concentration.
When more than about 15% of ECF volume is lost, renal conservation of sodium occurs; if the water losses continue, hypernatremia develops. The presence of volume deficits is indicated by the signs of IVV depletion, as previously described. Urine flow rate usually is less than 35 mL/h.
Solute Diuresis
The amount of water that must accompany the excretion of a given amount of solute in the urine is determined by the osmolality of the renal medullary interstitial fluid (with which the collecting duct fluid must equilibrate) and the plasma level of ADH activity (which determines the permeability of the collecting duct to water and, therefore, the rate at which water moves from the collecting duct to medullary interstitial fluid to achieve osmotic equilibrium). Hypernatremia results if water intake does not keep pace with renal water losses, because although renal sodium excretion also is increased in solute diuresis, renal sodium reabsorption is affected proportionately less than is water reabsorption. Large amounts of mannitol infused intravenously or high-protein mixtures fed by nasogastric tube (each gram of protein yields 8 mOsm as urea, phosphate, and potassium) can cause a solute diuresis sufficient to cause hypernatremia if water intake is inadequate. In solute diuresis, urine volume usually is greater than 35 mL/h.
Hypernatremia Associated with Formation of Dilute Urine
The finding of hypernatremia in combination with isotonic or hypotonic urine indicates that, at least in part, the hypernatremia results from failure of normal renal conservation of water. Failure to concentrate the urine under these conditions may result from the lack of ADH (hypothalamic-pituitary diabetes insipidus) or impaired renal tubular function that interferes with the development of a hypertonic medullary interstitium (renal tubular damage).
 FIGURE 10.2 Approach to the assessment of a hypernatremic patient. This approach does not consider patients with hypernatremia secondary to excessive administration of hypertonic saline. ADH, antidiuretic hormone. |
Central diabetes insipidus or nephrogenic diabetes insipidus should be suspected immediately in a patient with hypernatremia when the urine is very dilute (a Uosm😛osm ratio <0.5, or specific gravity <1.005).
In patients with renal tubular damage, the ability to concentrate and dilute the urine is decreased. As a result, under all conditions, the urine is isotonic or nearly isotonic with plasma. Hypernatremia can supervene when water losses exceed sodium losses and water intake does not keep pace with water losses. Despite the hypernatremia, significant sodium deficits usually are present because renal sodium wasting also usually is a feature of these disorders. The following sections are examples of clinical situations in which renal tubular damage can be associated with hypernatremia.
Diuretic Phase of Acute Renal Failure
Occasionally, in a patient recovering from acute renal injury, tubular function is more severely affected than is glomerular function. Thus, an inordinately large fraction of the glomerular filtrate escapes reabsorption, resulting in high urine flow rates. The period of inappropriate diuresis can persist for a few days to several weeks.
Postobstructive Diuresis
The sudden release of chronic urinary tract obstruction often is followed by several days or weeks in which urine flow rates are abnormally high. Shortlived nephrogenic diabetes insipidus develops in some patients.
MANAGEMENT OF WATER AND ELECTROLYTE BALANCE
Water requirements should be carefully monitored, especially in hospitalized patients. Patients with known fluid deficits or excesses should be approached as demonstrated in Tables 10.3
and 10.4. Minimum maintenance requirements can be calculated from two simple formulas.
and 10.4. Minimum maintenance requirements can be calculated from two simple formulas.
TABLE 10.3 General Guidelines for Planning Fluid and Electrolyte Therapy in Complicated Cases | ||||||||||||||||||||||
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