• BIOCHEMICAL INDICES OF WATER-MINERAL
METABOLISM
• Patients may develop lethargy, weakness, confusion, delirium, and seizures, especially in the presence of an abnormal serum sodium concentration.
• Muscle weakness occurs in patients with severe hypokalemia, hyperkalemia, and hypophosphatemia;
• Сonfusion, seizures, and coma may develop in those with severe hypercalcemia.
• In addition to taking a careful history, the diagnosis and treatment of fluid and electrolyte disorders are based on:
• 1) assessment of total body water and its distribution
• 2) serum electrolyte concentrations• 3) urine electrolyte conntrations • 4) serum osmolality
Body Water• Two-thirds of total body water (40 % of body
weight) is intracellular fluid (ICF), while one-third (20 % of body weight) is extracellular fluid (ECF).
• Water may be lost from either or both of the fluid compartments.
• One -fourth of extracellular fluid (5% of body weight) is retained within the blood vessels as plasma (effective circulating volume)
• Effective circulating volume may be assessed by physical examination (blood pressure, pulse rate, jugular vein dilation).
Serum Electrolytes
Evaluation of Urine• Fractional excretion (Fe) of an
electrolyte X (Fex) is calculated using a random urine sample with simultaneously obtained serum samples for X and creatinine (Cr).
• Fex(%) = UrineX/SerumX × 100 Urine Cr/Serum Cr
Serum Osmolality• Serum osmolality (normally 285-295
mosm/kg) can be calculated from the following formula:
• Osmolality = 2(Na+ mEq/L) + Glucose mg/dL + BUN mg/dL 18 2.8
• "Osmoles per kilogram of water" is osmolality; "osmoles per liter of solution" is osmolarity.
HYPONATREMIA
• Hyponatremia (defined as a serum sodium concentration less than 130 mEq/L) is the most common electrolyte abnormality observed in a general hospitalized population, seen in about 2 % of patients.
• Isotonic hyponatremia can be seen with hyperlipidemia and hyperproteinemia. Because of marked increases, lipids (chylomicrons, triglycerides, which make the blood visibly lipemic, and very occasionally cholesterol, which may not make the blood visibly lipemic) and proteins (> 10 g/dL, eg, intravenous immunoglobulin therapy) occupy a disproportionately large portion of the plasma volume.
• Plasma osmolality remains normal because its measurement is unaffected by the lipids and proteins.
• Because the sodium concentration in the plasma water is actually normal, hyperlipidemia and hyperproteinemia cause so-called "pseudohyponatremia."
• Hypertonic hyponatremia is most commonly seen with hyperglycemia.
• When blood glucose becomes acutely elevated, water is drawn from the cells into the extracellular space, diluting the serum sodium.
• The plasma sodium level falls 2 mEq/L for every 100 mg/dL rise when the glucose concentration is between 200 and 400 mg/dL. If the glucose concentration is above 400 mg/dL, the plasma sodium concentration falls 4 mEq/L for every 100 mg/dL rise in glucose.
HYPERNATREMIA • An intact thirst mechanism usually
prevents hypernatremia (> 145 mEq/L). Thus, whatever the underlying disorder (eg, dehydration, lactulose or mannitol therapy, central and nephrogenic diabetes insipidus), excess water loss can cause hypernatremia only when adequate water intake is not possible, as with unconscious patients
• A. Symptoms and Signs• When dehydration exists, orthostatic
hypotension and oliguria are typical findings. Because water shifts from the cells to the intravascular space to protect volume status, these symptoms may be delayed. Hyperthermia, delirium, and coma may be seen with severe hyperosmolality.
• B. Laboratory Findings• 1. Urine osmolality > 400 mosm/kg. Renal
water-conserving ability is functioning.• a. Nonrenal losses. Hypernatremia will
develop if water ingestion fails to keep up with hypotonic losses from excessive sweating, exertional losses from the respiratory tract, or through stool water. Lactulose causes an osmotic diarrhea with loss of free water.
• b. Renal losses. Whereas diabetic hyperglycemia can cause pseudohyponatremia, progressive volume depletion from the osmotic diuresis of glycosuria can result in true hypernatremia. Osmotic diuresis can occur with the use of mannitol or urea.
• 2. Urine osmolality < 250 mosm/kg. A dilute urine with osmolality less than 250 mosm/kg with hypernatremia is characteristic of central and nephrogenic diabetes insipidus. Nephrogenic diabetes insipidus, seen with lithium or demeclocycline therapy, after relief of prolonged urinary tract obstruction, or with interstitial nephritis, results from renal insensitivity to ADH.
Choice of Type of Fluid for Replacement
• Hypernatremia with hypovolemia—Severe hypovolemia should be treated with isotonic (0.9%) saline to restore the volume deficit and to treat the hyperosmolality, since the osmolality of isotonic saline (308 mosm/kg) is often lower than that of the plasma. This should be followed by 0.45% saline to replace any remaining free water deficit.
• Hypernatremia with euvolemia—Water drinking or 5% dextrose and water intravenously will result in excretion of excess sodium in the urine. If die GFR isdecreased, diuretics will increase urinary sodium excretion but may impair renal concentrating ability, increasing the quantity of water that needs to be replaced.
• Hypernatremia with hypervolemia—Treatment consists of providing water as 5% dextrose in water to reduce hyperosmolality, but this will expand vascular volume. Thus, loop diuretics such as furosemide (0.5-1 mg/kg) should be administered intravenously to remove the excess sodium. In severe renal insufficiency, hemodialysis may be necessary.
HYPOKALEMIA• A. Symptoms and Signs• Muscular weakness, fatigue, and muscle
cramps are frequent complaints in mild to moderate hypokalemia. Smooth muscle involvement may result in constipation or ileus. Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis may be seen with severe hypokalemia (< 2.5 mEq/L).
• B. Laboratory Findings• The electrocardiogram (ECG) shows
decreased amplitude and broadening of T waves, prominent U waves, premature ventricular contractions, and depressed ST segments. Hypokalemia also increases the likelihood of digitalis toxicity. Thus, in patients with heart disease, hypokalemia induced by certain drugs such as β2-adrenergic agonists and diuretics may impose a substantial risk
HYPERKALEMIA • Many cases of hyperkalemia are
spurious or associated with acidosis (Table 21-6). The common practice of repeatedly clenching and unclenching a fist during venipuncture may raise the potassium concentration by 1-2 mEq/L by causing acidosis and consequent potassium loss from cells
