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By Leon VandeCreek

ISBN-10: 1568870744

ISBN-13: 9781568870748

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B. Monitor serum potassium and the ECG for signs of hyperkalemia from excessive potassium therapy. c. If hypokalemia is caused by diuretic therapy or gastrointestinal fluid losses, measure and replace other ions such as magnesium, sodium, and chloride. G. Renal failure. Examples of drugs and toxins causing renal failure are listed in Table I–28. Renal failure may be caused by a direct nephrotoxic action of the poison or acute massive tubular precipitation of myoglobin (rhabdomyolysis), hemoglobin (hemolysis), or calcium oxalate crystals (ethylene glycol); or it may be secondary to shock caused by blood or fluid loss or cardiovascular collapse.

Because the pulse rate may be profoundly slow (10/min) and weak, perform careful cardiac evaluation before assuming that the patient is in cardiac arrest. Do not treat bradycardia; it will resolve with rewarming. 3. Unless the patient is in cardiac arrest (asystole or ventricular fibrillation), rewarm slowly (using blankets, warm intravenous fluids, and warmed-mist inhalation) to prevent rewarming arrhythmias. 4. For patients in cardiac arrest, usual antiarrhythmic agents and direct current countershock are frequently ineffective until the core temperature is above 32–35 °C (90–95 °F).

The serum blood urea nitrogen (BUN) is usually low (< 10 mg/dL). (2) Psychogenic polydipsia, or compulsive water drinking (generally > 10 L/d), causes reduced serum sodium because of the excessive free-water intake and because the kidney excretes sodium to maintain euvolemia. The urine sodium level may be elevated, but urine osmolality is appropriately low because the kidney is attempting to excrete the excess water and ADH secretion is suppressed. (3) Beer potomania may result from chronic daily excessive beer drinking (> 4 L/d).

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Innovations in Clinical Practice: A Source Book by Leon VandeCreek

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