-------------------------------------------------------------------------- TITLE: Fluid and Electrolyte Balance SOURCE: Dept. of Otolaryngology, UTMB, Grand Rounds DATE: 2 February 1991 RESIDENT PHYSICIAN: Eric W. Bridges, M.D. FACULTY: Francis B. Quinn, Jr., M.D. DATABASE ADMINISTRATOR: Melinda McCracken, M.S. -------------------------------------------------------------------------- "This material was prepared by resident physicians in partial fulfillment of educational requirements established for the Postgraduate Training Program of the UTMB Department of Otolaryngology/Head and Neck Surgery and was not intended for clinical use in its present form. It was prepared for the purpose of stimulating group discussion in a conference setting. No warranties, either express or implied, are made with respect to its accuracy, completeness, or timeliness. The material does not necessarily reflect the current or past opinions of members of the UTMB faculty and should not be used for purposes of diagnosis or treatment without consulting appropriate literature sources and informed professional opinion." I. Normal distribution of body fluids A. Total body water -50 to 70% of the body is composed of water; however, fat contains less water than skeletal therefore females and the obese have a lower percentage of their body weight as water. -the total body water is divided into three functional compartments: 1) the intracellular compartment which accounts for 30 to 40 percent of body weight, 2) the extracellular compartment, which can be subdivided into the intravascular or plasma compartment (5 percent of body weight) and 3) the interstitial compartment which makes up 15 percent of the body weight. B. Compartment composition -in the extracellular fluid, the predominate cation is sodium and the predominate anions are chloride and bicarbonate. -in the intracellular fluid, the predominate cation is potassium, while the predominate anions are phosphate and sulfate (see figure 4). C. Water movement between compartments 1. Osmolality -the amount of water in a compartment is determined by the number of osmotically active particles within that compartment. -because all cell membranes are freely permable to water, osmotic pressure in all compartments is the same and any condition which alters the osmotic pressure in one compartment will result in a redistribution of water to restore the balance. 2. Fluid shifts a. nonisotonic shifts -when the intracellular or extracellular compartment osmolality changes, water moves along the osmotic gradient from the hypotonic compartment to the hypertonic compartment until a new equilibrium is reached. The changes in various volume and concentration parameters with fluid shifts is summarized in table 1. b. isotonic shifts -result in change in intracellular water or concentrations because no osmotic gradient from intra- to extra-cellular. c. Starling forces -those gradients which promote fluid exchange between the plasma and interstitial fluid, which include the difference between capillary osmotic pressure and tissue (interstitial) osmotic pressure, and capillary hydrostatic pressure and tissue hydrostatic pressure. 3. Calculation of osmolality -plasma osmol. = 2*[sodium]+glucose/18+BUN/2.8 II. Normal fluid and electrolyte balance -the water, sodium, and potassium in a normal adult patient is summarized in table 2. III. Intravenous fluid therapy A. Maintenance therapy 1. Water 24 hour intravenous fluid requirements for adults and children are: 0 - 10 kg = 100 ml/kg 10 - 20 kg = 1000 ml + 50 ml/kg for every kg above 10 >20 kg = 1500 ml + 20 ml/kg for every kg above 20 2. Sodium -requirements are 1-2 mEq/kg/d in adults and 1-2 mEq/kg/d in children. This amount of sodium will replace obligatory sodium losses and suppress aldosterone secretion enough to prevent potassium wasting. 3. Potassium -obligatory losses are approximately 40 to 60 mEq per day in an adult, therefore, replacement with 0.5 to 1 mEq/kg/d is usually enough to maintain potassium balance in a patient with normal kidneys. 4. Other electrolytes -supplement as indicated by clinical assessment and laboratory testing. 5. Standard IV solutions (see table 3) B. Replacement of previous fluid losses 1. Hemodynamically unstable patient -treatment geared toward preventing or correcting shock. a. Crystalloid 1) Distribution -to expand the intravascular space, isotonic solutions must be used. Only 1/4 to 1/3 of the fluid remains intravascular. 2) Complications -large amounts of crystalloid lead to peripheral edema. -large amounts of normal saline may lead to hyperchloremic metabolic acidosis. -large amounts of lactated Ringer's given in the setting of hypovolemia and metabolic alkalosis may exacerbate the alkalosis when the lactate is metabolized. 3) Indications -initial therapy for acute hypovolemia and shock. b. Colloid -albumin, hespan, PRBC, plasma exert some degree of intravascular pressure. -the use of colloid solutions is directed towards augmenting the body's own response of releasing albumin from the liver (up to 50 gm or 40% of the normal intravascular pool) into the intravascular pool within 3 hours of the onset of hypovolemia. 1) Distribution -stay mainly within the vasculature provided capillary integrity is intact. 2) Complications -risk of pulmonary edema and respiratory failure, especially in patients with leaky capillaries. -more costly than crystalloid solutions -risk of anaphylactic or transfusion reactions, interference with coagulation. 3) Indications a) severe hypovolemia -if the hypovolemic state persists or returns after the administration of 2 liters of crystalloid in adults or 3 boluses of 20 ml/kg of crystalloid in children. b) low effective circulating volume with total body excess of sodium and water -for example, patients with ascites, CHF, post-cardiac bypass patients. c) metabolic hypoalbuminemia -liver transplants, hepatic resections, malnutrition, and liver disease. d) severe hemorrhage or coagulopathy -replace with PRBCs and FFP. 2. Hemodynamically stable patient -once intravascular volume has been restored or in patients who are dehydrated but not in shock, volume deficits can be corrected slowly over 24 to 36 hours with 1/2 the deficit replaced in the first 8 hours and the remaining half over the ensuing 16 - 28 hours. C. Ongoing volume losses 1. Fever -each degree centigrade above 37 C adds 2-2.5 ml/kg/d of insensible water loss. D5W 1/4 NS plus 5 mEq KCl/L is the best replacement fluid to approximate sweat. 2. Loss of body fluids a. Gastric -replace with D5W 1/2 NS plus 20 mEq KCl/L. If metabolic alkalosis is present, increase potassium to 40 mEq KCl/L. b. Biliary and pancreatic losses -replace with lactated Ringer's. Extra bicarbonate may be needed when replacing pancreatic losses. c. Small bowel and colon -replace with lactated Ringer's +/- 10 mEq KCl/L. 3. Third space losses -replace with lactated Ringer's. Approximately one liter of fluid for each quadrant of the abdomen involved in adults and 25 percent of the maintenance fluid for each quadrant in children. 4. Burns 5. Osmotic diuresis -due to elevated urea, glucose, or administered mannitol. Check urine electrolytes to guide replacement therapy if indicated. D. Goals of fluid therapy 1. Vital signs -tachycardia, decreased pulse pressure, and orthostatic hypotension are early signs of hypovolemia. Systolic blood pressure is not reliably lowered until 20 - 30% of the blood volume has been lost. 2. Physical examination findings a. neck veins - poor man's CVP b. lungs-crackles suggest volume overload or CHF c. heart-presence of S3 suggests volume overload d. periphery-edema suggests volume overload. Poor tissue turgor, dry mucous membranes, and cool extremities suggest hypovolemia. 3. Intake, output, and weights-one of the more accurate ways to assess fluid status. 4. Urine output-0.5-1.5 ml/kg/hr. Rates lower than this suggest renal failure, low flow states (prerenal azotemia), or hypovolemia. Rates higher than this suggest overhydration, diabetes insipidus, osmotic diuresis, or post-obstructive diuresis. 5. Laboratory data-electrolytes should be determined frequently in ICU patients, both to guide future therapy and prevent iatrogenic abnormalities. BUN/creatinine ratios can assist with hydration assessment with ratios <15 implying adequate hydration while ratios >20 imply low flow states. Urine electrolyte and urine osmolarity can assist with volume status if obtained before diuretic use or at least 12 hours after the last diuretic use. 6. Invasive monitoring-patients with multiple complex problems may require a balloon-directed pulmonary artery catheter (Swan-Ganz) to assist with fluid balance. IV. Electrolyte disturbances - diagnosis and treatment A. Hyponatremia 1. Evaluation and differential diagnosis -initial evaluation consists of obtaining a serum osmolality. a. Hypertonic -Posm > 305 mOsm/kg, usually due to hyperglycemia or hypertonic infusion (mannitol, glucose, glycine). Sodium fall 1.6 mEq/L for each 100 mg/dL increase in glucose or mannitol. b. Isotonic -Posm 278 - 305 mOsm/kg, usually secondary to hyperlipidemia, hyperproteinemia, or isotonic infusions of glucose, mannitol, or glycine. c. Hypotonic -Posm < 278 mOsm/kg, divided into three categories based on volume status or hypervolemic, hypovolemic, or euvolemic (see table 6). 1) hypervolemia 2) hypovolemia 3) euvolemia 2. Symptoms -include confusion, anorexia, lethargy, nausea, vomiting, coma, and seizures. Severity of symptoms depend on the rate of fall of sodium as well as the absolute level of sodium. Symptoms usually do not develop before sodium concentrations fall to 120 - 125 mEq/L. 3. Treatment a. Asymptomatic hyponatremia 1) hypertonic or isotonic-correct underlying disorder, insulin if hyperglycemia. 2) hypervolemic hypotonic-water restriction, consider diuresis. 3) hypovolemic hypotonic-isotonic saline. 4) euvolemic hypotonic-water restriction of <500 ml/day. b. Symptomatic hyponatremia-requires more aggressive treatment with 3% NaCl to correct the sodium deficit no faster than 2 mEq/hr to a concentration of 120 - 125 mEq/L. Rate of administration is (2)(0.6)(body weight in kg)/(513) = ml 3% NaCl per hour. Underlying cause of hyponatremia should be sought and aggressively treated. B. Hypernatremia 1. Evaluation and differential diagnosis -always associated with elevated serum osmolality. -first evaluate volume status, categorize as hypervolemic, hypovolemic, or euvolemic. -careful history and physical with electrolytes, BUN, creatinine, urine sodium and urine osmolality will help make diagnosis and underlying cause. -in the ICU setting, the most common causes are iatrogenic and diabetes insipidus. 2. Signs and symptoms -depends upon rate of development of abnormality and volume status of patient. -neurologic abnormalities most frequently seen and include: restlessness, lethargy, twitching, tremulousness, ataxia, seizures, dementia, delirium and strokes secondary to subarachnoid and subcortical hemorrhages. This is due to cellular dehydration and stretching of cerebral bridging veins. Also may note red swollen tongue, flushed skin, tachycardia, reduced blood pressure, and core temperature elevation. 3. Treatment -depends on extracellular volume status and rate of development of abnormality. a. Extracellular volume status (see table 5) 1) hypovolemia-first restore volume statue with isotonic saline or lactated Ringer's until euvolemic, then 1/4 NS or D5W. The water deficit can be calculated by: (0.6)(body wt in kg)((current Na/140)-1)=deficit in L in cases of DI, SQ pitressin 5U every 4-6 hr or a pitressin drip of 1 U/hr titrated to give urine output of 100-200 ml/hr may be necessary. 2) hypervolemia-Lasix with D5W or D5 1/4 NS. In renal failure, dialysis may be required to remove fluid. 3) euvolemia-water replacement orally or D5W parentally. b. Rate of correction 1) acute hypernatremia-with symptoms, correct rapidly over several hours. Without neurologic symptoms, treat as chronic. 2) chronic hypernatremia-because brain can compensate to slowly developing hypernatremia by creating idiogenic osmoles to prevent cell shrinkage, rapid correction would lead to cerebral swelling and edema. Should correct slowly over 48 hours, no faster than two mOsm/hr. C. Hypokalemia 1. Evaluation-most potassium is intracellular (65 mEq in serum vs. 4000 mEq intracellularly), therefore, hypokalemia can result from altered transcellular distribution, total body depletion of potassium or a combination of both. Evaluation needs to include an electrocardiogram. 2. Differential diagnosis -history and physical, acid-base status, and urine electrolytes are useful in determining the etiology. a. Secondary to redistribution-respiratory and metabolic alkalosis, exogenous bicarbonate, insulin and glucose. For every 0.1 unit change in pH, there will be a 0.6 mEq/l change in K+. b. Gastrointestinal losses-urine K+<20 mEq/day, include diarrhea, intestinal or biliary fistulas, villous adenomas, laxative abuse, vomiting or NG suction. Urine K+ in the last two disorders may be greater than 20 mEq/day due to the increased potassium excretion that occurs with alkalosis. c. Renal losses-urine K+>20 mEq/day, includes renal tubular acidosis, diuretic phase of ATN, post- obstructive diuresis, osmotic diuresis, diuretics, corticosteroids, hyperaldosteronism, or Cushing's syndrome. d. Poor intake-prolonged administration of potassium- free parenteral fluids or insufficient oral intake. 3. Signs and symptoms a. Cardiac-increased incidence of dysrhythmias especially PACs. VPBs also seen, and increased digitalis toxicity. Presence of U waves, flattened or inverted T waves seen in moderate hypokalemia, progresses to S-T depression, prolonged P-R interval, tall P waves and widened QRS complexes. b. Neuromuscular-intestinal ileus, constipation, rhabdomyolysis, weakness and paralysis. Respiratory arrest may occur with very low K+. c. Renal-decreased GFR, increased ammonium production metabolic alkalosis. d. Endocrine-decreased aldosterone and insulin release, increased renin release. 4. Treatment -serum potassium should be confirmed and adequate urine output present. If the GI tract is working, oral supplementation preferred. Deficits can be replaced at 80 - 120 mEq/day. -if the gut is not working or the hypokalemia is severe, KCl should be given IV mixed with saline without dextrose. Can be given by peripheral vein up to 10 mEq/hr. Rates of 20 mEq/hr to 40 mEq/hr require central venous administration and continuous cardiac monitoring. D. Hyperkalemia 1. Evaluation-best made with an EKG with peaked T waves and a widened QRS complex. 2. Differential diagnosis-careful history and physical, EKG, blood chemistry, and arterial blood gas are helpful in determing etiology. a. Redistribution-seen in setting of acidosis. b. Decreased potassium excretion-usually seen in acute renal failure and adrenal insufficiency. Less common in chronic renal failure unless challenged with a potassium load. c. Increases potassium load-may be endogenous to tissue breakdown such as major surgery, crush injury, rhabdomyolysis, massive hemolysis or GI bleeding, transfusions especially when stored for extended periods, and high dose penicillin. d. Pseudohyperkalemia-occurs secondary to a hemolyzed blood sample, or in patients with leukemic WBC counts or thrombocytosis >750,000. The diagnosis is confirmed by a normal EKG and normal potassium on heparinized blood sample. 3. Signs and symptoms a. Cardiac-altered conduction leading to arrest. Rare to see alterations other than peaked T waves until K+ reaches 6.5 mEq/L. b. Neuromuscular-tingling, malaise, weakness, paresthesias, and paralysis. c. Endocrine-increased aldosterone and insulin. 4. Treatment-rule out pseudohyperkalemia first. a. K+<6.5 mEq/l and no EKG changes-stop all supplemental potassium, check potassium. b. K+<6.5 mEq/l with EKG changes-stop all supplemental K+, give Kayexalate PO or PR per table 7. Search for underlying cause and correct. c. K+>6.5 mEq/l or any K+ level with marked EKG changes-stop all potassium and aggressive measures as outlined in table 7. E. Hypocalcemia 1. Evaluation -calcium exists in various forms in the body; 50% is free or ionized (this is the physiologically active form), 40% is bound to proteins, and 15-20% is bound to anions such a citrate or phosphate. Serum albumin should be measured concurrently to rule out pseudo- hypocalcemia; the calcium falls 0.8 mg/dL for each 1 gm/dL fall in albumin below 4.0. Ideally, the diagnosis of hypocalcemia should be base on the ionized calcium level. 2. Differential diagnosis -the most common causes of hypocalcemia can be differentiated with a good history and physical. a. Hypoparathyroidism-surgical, neoplastic, or infiltrative. b. Pancreatitis c. Hypomagnesemia d. Hyperphosphatemia-renal, rhabdomyolysis. e. Hypovitaminosis D-chronic renal failure, malabsorption. f. Drugs and toxins-transfusions with citrated blood, gentamicin, protamine, mithramycin, dilantin, and phenobarbital. 3. Signs and symptoms a. Central nervous system-mental status changes, seizures, and extrapyramidal movement disorders. b. Neuromuscular-circumoral and acral paresthesias, tetany (carpo-pedal spasm, Chvostek's sign), myopathy. c. Cardiovascular-hypotension, increased Q-T interval, occasionally ventricular dysrhythmias. 4. Treatment (q.v. figure 2) a. Acute -patients with neuromuscular symptoms at risk for developing seizures and laryngospasm, therefore, give 200 - 300 mg of calcium. This is equivalent to 20 - 30 ml of 10% calcium gluconate or 5 - 10 ml of 10% calcium chloride. -should be given slowly IV over several minutes so as not to potentiate hypertension. -should not be given in the same line with NaHCO3 as it will precipitate out the calcium. -concomitant hyperphosphatemia and hypomagnesemia should be corrected. b. Chronic -asymptomatic treated with oral supplementation or adding calcium to maintenance IV fluid plus oral vitamin D. Question as to whether give calcium to asymptomatic post-thyroidectomy patients as hypocalcemia stimulates remaining parathyroid tissue to produce PTH. F. Hypercalcemia 1. Evaluation 2. Differential diagnosis a. Malignancy, hyperparathyroidism, and granulomatous disease account for 90% of cases of hypercalcemia. Other etiologies to be considered if these are not found include: thyrotoxicosis, Paget's disease, Addison's disease, immobilization, thiazide diuretics, milk-alkali syndrome, vit. D intoxication, vit. A intoxication, hypophosphatemia. -PTH should be measured, if low, then workup for occult malignancy, if high then search for parathyroid adenoma or hyperplasia. 3. Signs and symptoms (moans, bones, stones, groans) a. General-malaise, weakness, fatigue. b. Neuropsychiatric-lethargy, confusion, polydipsia, headache, decreased concentration and memory. c. Gastrointestinal-anorexia, nausea and vomiting, constipation. b. Renal-polyuria, nephrolithiasis, nephrocalcinosis, acute and chronic renal failure. c. Cardiovascular-bradycardia, heart block. 4. Treatment (q.v. figure 1) a. Initiation 1) Ca++ 11.5 - 12.5 mg/dl without symptoms-observe 2) Ca++ 11.5 - 12.5 mg/dl with symptoms-aggressive treatment. 3) Ca++ > 12.5 mg/dl-aggressive treatment. b. Hydration with sodium/calcium diuresis-normal saline with potassium 1 liter over an hour then 200 - 400 ml/hr until euvolemic. Then D5 1/2NS with 20 mEq KCl/L plus 8 mEq MgSO4/L at 200 ml/hr. Lasix 50 - 100 mg every 1 to 2 hrs to maintain urine output over 500 ml/hr. Monitor potassium, magnesium, calcium levels. c. Hemodialysis or peritoneal dialysis-used in patients with renal failure or life-threatening hypercalcemia. d. Mithramycin e. Diphosphonates (Didronel) f. Corticosteroids g. Phosphates h. Calcitonin i. urgent parathyroidectomy G. Hypophosphatemia 1. Evaluation -majority of phosphate in intracellular. -hypophosphatemia can occur secondary to external losses or redistribution from extracellular to intracellular pools. 2. Differential diagnosis -urine phosphate excretion may be helpful as <100 mg/d implies GI losses or redistribution while >100 mg/d implies renal losses. a. Gastrointestinal losses-inadequate intake, malabsorption, alcoholism, aluminum antacids, chronic diarrhea. b. Primary renal losses-primary hyperparathyroidism, diuretics, burns, alcoholism. c. Redistribution-glucose infusion, insulin administration, TPN or food administration after starvation, malnutrition, respiratory alkalosis, catecholamine administration. 3. Signs and Symptoms a. Central nervous system-obtundation, coma, seizures. b. Musculoskeletal-rhabdomyolysis, myopathy, weakness, cardiomyopathy and respiratory arrest. c. Hematopoietic-anemia. d. General-weakness, fatigue. 4. Treatment (1 mmole of phosphate = 31 mg elemental P) a. Severe life-threatening, phosphate < 1 mg/dl -administer 0.16 mmole/kg ( 5 mg/kg) over 6 hours. b. Phosphate = 1.0 - 2.0 mg/dl -administer 0.08 mmole/kg ( 2.5 mg/kg) over 6 hours. c. Dose modifiers -for above two situations, increase dose by 25- 50% if patient symptomatic, decrease dose by 25- 50% if patient hypercalcemic. d. Mild asymptomatic -phosphosoda 5 ml TID (4.2 mmole/ml). H. Hyperphosphatemia 1. Evaluation and differential diagnosis -unusual in patients with normal renal function. -three settings in which renal excretion insufficient to prevent hyperphosphatemia: a. Massive phosphate infusion 1) endogenous-cytotoxic therapy, rhabdomyolysis. 2) exogenous-phosphate enemas, laxative abuse. b. Decreased glomerular filtration rate 1) acute renal failure 2) chronic renal failure c. Increased tubular reabsorption 1) hypoparathyroidism 2) thyrotoxicosis 3) hypovolemia 4) excess growth hormone 5) tumoral calcinosis 2. Signs and symptoms -usually related to hypocalcemia that develops with complexing of calcium to phosphate in insoluble forms. 3. Treatment a. acute-resolves in 12 hours with normal renal function. If hypocalcemic symptoms present, Diamox (acetazolamide) 15 mg/kg q3-4 hr may help but usually dialysis is required. b. mild or chronic-seen in chronic renal failure or neoplastic calcinosis, treated with low phosphate diet and aluminum antacids which bind phoshate. I. Hypomagnesemia 1. Evaluation-often by disturbances in calcium and potassium balance. -consider hypomagnesemia in hypokalemic patients, hypocalcemic patients, alcoholism, post-chemotherapy, intractable arrhythmias, chronically ill or malnourished patients. 2. Differential diagnosis a. malabsorption b. chronic diarrhea-IBD, laxative abuse, intestinal infection. c. alcoholism-secondary to malnutrition and renal effects. d. low intake-malnutrition, prolonged IV therapy. e. large GI fluid losses-fistulas, NG suction, prolonged vomiting. f. increased urinary excretion of Mg++-secondary to drugs such as cisplatin, digoxin, aminoglycosides, amphotericin B and diuretics. 3. Signs and symptoms a. Neuromuscular-paresthesias, tremors, weakness, vertigo, ataxia, nystagmus, seizures and coma. b. Psychiatric-mood alterations, psychosis. c. Cardiovascular-ventricular arrhythmias resistant to conventional treatment, predisposed to digitalis toxicity. d. Gastrointestinal-anorexia, vomiting, dysphagia. e. Hematopoietic-anemia. 4. Treatment a. acute-if symptomatic, give 2gm MgSO4 as 20% solution IV over 2 to 5 minutes. Follow with 10 gm over the next 24 hours if renal function OK. Four to six gm per day for the next 4 - 5 day should restore body stores. Intravenous magnesium can cause hypotension, therefore, check blood pressure. b. chronic-in symptomatic patients, 3 - 6 gm orally for 3 days should restore body stores. c. prophylactic-1 to 2 gm per day in IV fluid can prevent hypomagnesemia in ill patients with normal renal function. J. Hypermagnesemia 1. Evaluation and differential diagnosis -minor elevations (less than 4 mEq/L) have been reported with lithium therapy, bony metastases, hypothyroidism, viral hepatitis, and acute acidotic states. Most cases follow a combination of impaired renal function and administration of magnesium containing drugs (antacids). 2. Signs and symptoms -earliest sign is loss of deep tendon reflexes, others include hypotension, nausea/vomiting, cutaneous flushing, and bradycardia. Respiratory depression can occur at very high levels (>12 mEq/L) as can cardiac asystole. 3. Treatment a. calcium-100 to 200 mg IV as gluconate or chloride over 5 to 10 minutes will transiently reverse symptoms/toxicity. b. dialysis-necessary if renal function poor. c. removal of Mg++ source d. prevention-avoid magnesium containing compounds in patients with renal failure. ---------------------------------------------------------------------------- BIBLIOGRAPHY 1. Lyerly, H.K. The Handbook of Surgical Intensive: Practices of the Surgery Residents at the Duke University Medical Center. Chicago: Yearbook Medical Publishers, 1989. 2. West, J.B. ed. Physiological Basis of Medical Practice. Baltimore: Williams & Wilkins, 1985. 3. Pestana, C. Fluids and Electrolytes in the Surgical Patient. Baltimore: Williams & Wilkins, 1985. 4. Schrock, T.R. Handbook of Surgery. Greenbrae, Calif.: Jones Medical Publications, 1985. 5. Economou, S.G., et al. Rush University Review of Surgery. Philadelphia: W.B. Saunders, 1988. 6. Shelly, M.P., Eltringham, R.J. Rational fluid therapy during surgery. British Journal of Hospital Medicine. 1988 June 39(6): 506-17. 7. Beck, L.H. Perioperative renal, fluid, and electrolyte management. Clinics in Geriatric Medicine. 1990 August 6(3): 557-69. 8. Scholten, D.J. Electrolytes and plasma volume regulation in hypovolemic shock. American Journal of Emergency Medicine. 1985 2(1):86-91. 9. Chesney, R.W., Zelikovic, I. Pre- and postoperative fluid management in infancy. Pediatrics in Review. 1989 November 11(5): 153-58. 10. Twigley, A.J., Hillman, K.M. The end of the crystalloid era? Anaesthesia. 1985 September 40(9): 860-71. ------------------------------------END------------------------------------------