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Quick Test posted on 3.11.10:
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Surgical Patient Electrolyte Abnormalities
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Combined water and electrolyte depletion may occur from gastrointestinal losses due to nasogastric suction, enteric fistulas, enterostomies, or diarrhea. Other causes are excessive diuretic therapy, adrenal insufficiency, profuse sweating, burns, and body fluid sequestration following trauma or surgery. Diagnosis of combined volume and electrolyte deficiency can be made from the history, physical signs, and records of intake and output. The clinical findings are similar to those of pure volume depletion. However, the urine Na+ concentration is often less than 10 meq/L, a manifestation of renal sodium conservation resulting from the action of aldosterone on the renal tubule. The urine is usually hypertonic (sp gr > 1.020), with an osmolality greater than 450–500 mosm/kg. The decreased blood volume diminishes renal perfusion and often produces prerenal azotemia, reflected by elevated blood urea nitrogen (BUN) and serum creatinine. Prerenal azotemia is characterized by a disproportionate rise of BUN compared to creatinine; the normal BUN/creatinine ratio of 10:1 is exceeded and may go as high as 20–25:1. This relationship helps differentiate prerenal azotemia from acute tubular necrosis, in which the BUN/creatinine ratio remains close to normal as the serum levels of both substances rise.
Combined water-electrolyte deficits are corrected by restoring volume and the deficient electrolytes. The magnitude of the volume deficit can be estimated by serial measurements of body weight, since acute changes in body weight primarily reflect changes in body fluid. Central venous or pulmonary artery pressure may be low in blood volume deficits and may be useful for monitoring replacement therapy.
The composition of the replacement fluid should take into account the PNa concentration: If the PNa is normal, fluid and electrolyte losses are probably isotonic, and the replacement fluid should be isotonic saline or its equivalent. Hyponatremia may result from salt loss exceeding water loss (ie, the decrease in Na+e will be greater than the decrease in TBW; equation 2) or from previous administration of hypotonic solutions. In this situation, the magnitude of the salt deficit can be calculated from equation 3.
Replacement therapy should be planned in two steps: (1) The sodium deficit should be calculated, and (2) the volume deficit should be estimated from clinical signs and changes in body weight. From these calculations, a hypothetical replacement solution can be devised in which the sodium deficit is administered as NaCl and the volume deficit as isotonic NaCl solution. Then administer isotonic NaCl solutions and monitor the patient's response (ie, urine volume and composition, serum electrolytes, and clinical signs). With restoration of ECF volume, renal perfusion improves, and excretion of water will occur while Na+ continues to be reabsorbed. When replacement is adequate, renal function and serum Na+ and Cl– concentrations will return to normal.
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| Fig. 76-3. Increased plasma osmolality causes a shift of water out of the intracellular compartment. Decreased cell volume impairs tissue function, particularly in the central nervous system. |
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Quick Test Questions QUESTION 1: A patient who has spasms in the hand
when a blood pressure cuff is blown up most likely has
QUESTION 2: Metabolic acidosis with a normal anion
gap is found in a patient with
QUESTION 3: The most common fluid disorder in the
surgical patient is
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