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As the major cation of the ECF and the major determinant of osmolality, sodium maintains the concentration and volume of the ECF. Normal sodium ranges from 135 to 145 mg/dL in most laboratories. Sodium maintains irritability and conduction in nerve and muscle tissue and assists in the regulation of acid-base balance. Since most diets have an excess of sodium, the kidney maintains normal levels through excretion of sodium and retention of free water.
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Shifts in fluid balance can lead to an increase in serum sodium and osmolality. This shift results in stimulation of thirst and an increase in antidiuretic hormone (ADH). In normal, alert individuals, hypernatremia is unlikely to occur.
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Hypernatremia is defined as a sodium level greater than 145 mEq/L. It is a relative state of free water deficit and an increase in the solute concentration in all body fluids. The 3 major hypernatremic states result from loss of water, hypotonic fluid loss, and sodium retention.
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Pure water loss usually occurs with increased insensible loss through the skin. Thermal burn injury is associated with the greatest risk of insensible water loss. Diabetes insipidus, which results in massive amounts of dilute urine output, can be seen in patients with severe preeclampsia.
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Figure 25-2 offers a simple algorithm for the treatment of hypernatremia due to this cause.
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Hypotonic fluid loss is the most common cause of hypernatremia. It is usually caused by dehydration due to gastroenteritis or an osmotic diuresis.
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Signs of ECF depletion may be present. Oliguria will be present unless the osmotic diuresis has been induced. Treatment is outlined in Fig 25-3.
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Sodium retention is an uncommon phenomenon. It is usually seen only when hypertonic saline- or bicarbonate-containing solutions are being infused.
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Central Diabetes Insipidus
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Central diabetes insipidus (CDI) is a unique cause of hypernatremia. It is most often seen in the setting of acute head injury, pituitary injury, or cerebral hemorrhages. Early recognition is the key to treatment. The diagnosis of CDI should be suspected if the urine is not concentrated in the setting of the hypernatremia.7
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Hyponatremia is defined as a serum sodium level of 135 mEq/L or less. Three major categories of hyponatremia exist: isotonic (pseudohyponatremia), hypertonic, and hypotonic. Severe hyponatremia (<120 mEq/L) is a serious life-threatening condition. Mortality rate may exceed 50%; however, rapid correction of sodium may produce central pontine myelinolysis and cerebral edema which can be fatal.
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Isotonic hyponatremia is characterized by a low serum sodium level but a normal plasma osmolality. Common causes include hyperproteinemic states and hyperlipidemic states. The management requires evaluation and correction of the underlying cause. The following correction factors may be used to assist in correcting the sodium concentration:
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Hypertonic hyponatremia is diagnosed by a low serum sodium and a plasma osmolality of greater than 290 mOsm/kg H2O. The most common cause of this disorder is hyperglycemia seen in association with diabetic ketoacidosis (see Chap 11). Correction of hyponatremia requires addressing the underlying disorder and replacing the free water deficit (Fig 25-3).
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Hypotonic hyponatremia is characterized by a low serum sodium and plasma osmolality. It can be divided into 3 subtypes: isovolemic, hypervolemic, and hypovolemic. The clinician should address 3 major concerns: The patient’s neurological status, volume status, and adrenal function.
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Isovolemic hyponatremia is characterized by a small gain in free water. This may be related to inappropriate secretion of ADH or in rare instances psychogenic polydipsia. Numerous drugs have been implicated in this disorder and they are listed as follows:
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Hypovolemic hyponatremia is characterized by the loss of fluid that is isotonic to plasma combined with volume replacement using a hypotonic fluid. This results in a net sodium loss. The most common causes of this disorder are diuretics, adrenal insufficiency, or diarrhea. A urine sodium can help to identify the etiology (ie, renal or extrarenal) of the hyponatremia.
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Hypervolemic hyponatremia occurs in patients in which there is excess water and sodium gain. Edema is common in this population. Causes include heart, renal, and liver failure. The evaluation and management of hypotonic hyponatremia is presented in Fig. 25-4.
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Potassium is the major intracellular cation. The normal plasma potassium concentration is 3.5 to 5.0 mmol/L. Renal excretion is the major route of elimination of dietary or other sources of excess potassium. The clinician should keep in mind that serum potassium may be falsely elevated in the presence of hemolysis or factitiously decreased when processing of a lab sample is delayed.
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Hypokalemia is defined as a serum potassium concentration below 3.5 mEq/L. The causes of hypokalemia may be classified as transcellular shift, as in the use of β agonist (ie, terbutaline), or from depletion. The major causes of the latter are renal loss, most commonly caused by diuretic therapy, or extrarenal, usually seen with excessive diarrhea. A number of drugs listed below are also associated with hypokalemia. Treatment is outlined in Fig 25-5.
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Hyperkalemia is defined as serum potassium above 5.5 mEq/L. It is caused by the release of potassium into the extracelluar fluid such as in myonecrosis, or by reduced renal excretion.8
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Hyperkalemia can be associated with fatal cardiac arrythmias; therefore, it should be treated much more aggressively than hypokalemia (Fig 25-6).
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Magnesium is not uniformly distributed in the body fluid compartments. Over half of the total body stores are located in the bone and less than 1% are distributed in plasma. This distribution creates a problem in diagnosing disturbances in magnesium balance. Magnesium levels are frequently overlooked in the critically ill patient and are not often replaced. For these reasons, magnesium may be the most common electrolyte abnormality in critically ill patients. In obstetrics, the use of magnesium for tocolysis and for neuroprophylaxis can further complicate the picture. The most common cause of magnesium depletion in our population is the use of diuretics.
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The use of amnioglycosides can also lower magnesium levels. Alcoholism is a rare cause of magnesium depletion in obstetric patients. Low levels of magnesium may potentiate cardiac arrythmias.
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Hypermagnesemia is almost always associated with renal insufficiency, with excess magnesium intake, or in cases of diabetic ketoacidosis. Infusion of magnesium in patients with preeclampsia or other diseases that may be associated with renal insufficiency should be done with care. Hypotension can be seen with magnesium levels of 3.0 to 5.0 mEq/L. A level greater than 12 mEq/L can be associated with respiratory depression. Levels greater than 14 mEq/L can be associated with cardiac arrest. Treatment protocols are outlined in Table 25-6.
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Calcium and Phosphorus Balance
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There are 3 fractions of calcium in the blood. About 50% of calcium is bound to serum proteins—with albumin accounting for 80% of protein binding. Anions like bicarbonate are bounded by 5% to 10% of calcium. The remainder of calcium is present as the free or “ionized” form of calcium. The interpretation of calcium levels must be adjusted for change in serum albumin.
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A correction factor, that increases the total calcium by 0.8 mg/dL for each 1 mg/dL decrease in albumin, should be used. Obtaining an ionized calcium may avoid using the above correction factor; however, changes in pH or other factors may also alter calcium levels.
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The most common cause in an acute care setting is magnesium depletion. Other causes such as hypoparathyroidism are usually not a concern in an acute setting. Massive transfusion, pancreatitis, and burns are other causes of decreased calcium level in this patient population.
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The clinical manifestations include neuromuscular excitability, which may vary, cardiovascular excitability including decreased myocardial contractility, and a prolonged QT interval. Treatment includes the infusion of calcium chloride or gluconate.9
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Hypercalcemia should be treated when the serum calcium level approaches 13 mg/dL or higher. Causes of hypercalcemia include malignancy and hyper-parathyroidism. Mental status changes are the most common clinical symptoms and warrant immediate therapy. The aim of the therapy is to facilitate the excretion of calcium in the urine (Table 25-7).
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Like magnesium and potassium, phosphorous is predominately an intracellular ion. While phosphorous levels may show diurnal variation, severe hypophosphotemia (serum level below 0.5 mg/dL) is uncommon. The most common causes of hypophosphotemia in the obstetric population are recovery from diabetic ketoacidosis, aluminum antacid use, or respiratory alkalosis. Phosphate deficiency reduces cardiac contractility, shifts the oxygen dissociation to the left, and may contribute to skeletal muscle weakness. Intravenous replacement is recommended (Table 25-8).
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Hyperphosphatemia is seen in the face of renal failure or tissue destruction, such as rhabdomyolysis. Management is directed at correcting the underlying problem. Aluminum-containing antacids may also be administered (Table 25-8).