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COPYRIGHT 2004 Jannetti Publications, Inc.
Postoperative hyponatremia is a well-documented postoperative concern for certain surgical procedures, including transurethral resection of the prostate. The complications are serious, with profound effects on patient outcome. Proper management includes understanding high-risk procedures, pathophysiology, clinical symptoms, and treatment options.
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The anesthetic management of patients undergoing surgical procedures is an enormous responsibility involving adequate preoperative planning, perioperative management, and a postoperative evaluation of the patient's overall status. A common expectation of the anesthesia provider's postoperative evaluation is adequate pain control for the patient. However, there are many other areas in which the expertise of the provider can make a tremendous difference in patient outcome. The focus of this manuscript is the phenomenon of postoperative hyponatremia.
Definition and Classifications
Hyponatremia is defined as a serum sodium concentration of less than 135 mEq/L (McCance & Huether, 2002). This sodium deficit usually causes a hypoosmolar state that is implied to pertain to all body fluid compartments. However, it must be understood that hyponatremia as an isolated finding does not offer a conclusion as to the patient's total body sodium content or volume status (Longnecker, Tinker, & Morgan, 1998). This leads us to the various classifications of hyponatremia and their possible causes.
Hyponatremia as a pure deficit of sodium can be caused by an inadequate intake of dietary sodium. This particular cause of hyponatremia is a rare occurrence but it can occur in individuals on sodium-restriction diets, especially if they are under diuretic therapy. The use of diuretics (without sodium restriction), vomiting, diarrhea, gastric suctioning, and burns are other potential causes of hyponatremia (McCance & Huether, 2002).
Dilutional hyponatremia, an excess of total body water in relation to total body sodium, can be a result of the excessive administration of hypotonic intravenous fluids, excessive intake of water orally (either to relieve thirst or due to psychogenic polydipsia), tap water enemas, renal water retention, or syndrome of inappropriate antidiuretic hormone (SIADH) secretion. It must be noted that despite the hyponatremia, in this classification, the total body sodium content may be increased, decreased, or unchanged (McCance & Huether, 2002).
Hypertonic hyponatremic state develops with hyperlipidemia, hyperproteinemia, and hyperglycemia. This class of hyponatremia is characterized by a decrease in serum sodium concentration with a simultaneous increase in serum osmolality (Longnecker et al., 1998). The subsequent increase in plasma lipids, proteins, and glucose causes a shift of water volume to the extracellular fluid compartment. This fluid shift leads to the dilution of sodium concentration (Longnecker et al., 1998).
Clinical Manifestations
Symptoms related to hyponatremia are primarily of a neurologic nature and result from an increase in intracellular water. The severity of the symptoms generally corresponds to the rate at which the hyponatremia develops. Frequently, patients with a serum sodium concentration of greater than 125 mEq/L are asymptomatic. Early symptoms include anorexia, nausea, and weakness; all of which are characteristically nonspecific.
Cerebral edema, a progressive consequence, results in lethargy, confusion, seizures, coma, and subsequently death. Serious symptoms can usually be seen when serum sodium concentrations are less than 120 mEq/L and it should be noted that premenopausal women seem to be at a greater risk for neurologic impairment and damage than men (Morgan, Mikhail, Murray, & Larson, 2002).
Patients with chronic hyponatremia or those developing the condition slowly are commonly asymptomatic. Neurologic symptoms in this group may be more related to changes in cell membrane potential than to changes in cell volume (Morgan...
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