Fluid and Electrolyte
Management of the Surgical Patient
BASIC SCIENCE QUESTIONS
1. What percentage of body weight is made up of water?
Water constitutes approximately 50 to 60% of total body weight. In an average young adult male 60% of total body weight is TBW, whereas in an average young adult female it is 50%. The lower percentage of TBW in females correlates with a higher percentage of adipose tissue and lower percentage of muscle mass. Estimates of percentage of TBW should be adjusted downward approximately 10 to 20% for obese individuals and upward by 10% for malnourished individuals. (See Schwartz 9th ed., pp 51 & 52.)
2. Which of the following is the largest fluid compartment in the body?
B. Central spinal fluid
C. Interstitial fluid
D. Intracellular fluid
Intracellular fluid is the largest fluid compartment in the body and makes up approximately 40% of total body weight (Fig. 3.1). Extracellular fluid, which is composed of plasma and interstitial fluid, makes up 20% of body weight. Central spinal fluid is a very small fluid compartment, composed mostly of plasma. (See Schwartz 9th ed., p 52; See Fig. 3-1.)
FIG. 3-1. Functional body fluid compartments. TBW = total body water.
3. Which of the following is the cation present in largest amounts in intracellular fluid?
Potassium is the most common cation present in intracellular fluid (Fig. 3-2). Sodium is the most common cation present in extracellular fluid (plasma and interstitial fluid). Calcium is virtually absent in intracellular fluid, and is present only in small amounts in extracellular fluid. Chloride is an anion. (See Schwartz 9th ed., p 52; See Fig. 3-2.)
FIG. 3-2. Chemical composition of body fluid compartments.
1. If 1 liter of 0.9% NaCl solution is given intravenously, how much will be distributed to the interstitial space?
A. 100 cc
B. 250 cc
C. 400 cc
D. 750 cc
Sodium is confined to the extracellular fluid (ECF) compartment, and because of its osmotic and electrical properties, it remains associated with water. Therefore, sodium-containing fluids are distributed throughout the ECF and add to the volume of both the intravascular and interstitial spaces. Although the administration of sodium-containing fluids expands the intravascular volume, it also expands the interstitial space by approximately three times as much as the plasma.
One liter of normal saline will be distributed 3:1 to the interstitial space. Therefore, 750 ml will be distributed to the interstitial space and 250 ml will remain in the intravascular volume. (See Schwartz 9th ed., p 53.)
2. What is the approximate serum osmolality for a patient with the following laboratory findings?
Na 130 Cl 94 K 5.2 CO2 14 Glucose 360 BUN 84 Creatinine 3.2
The principal determinants of osmolality are the concentrations of sodium, glucose, and urea (blood urea nitrogen, or BUN): Calculated serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8)
For this patient: (130 × 2) + (360/18) + (84/2.8) = 264 + 20 + 30 = 310 (See Schwartz 9th ed., p 53.)
3. A patient develops a high output fistula following abdominal surgery. The fluid is sent for evaluation with the following results: Na 135 K 5 Cl 70. Which of the following is the most likely source of the fistula?
B. Small bowel
D. Biliary tract
The composition of pancreatic secretions is marked by a high level of bicarbonate (HCO3−). (Table 3-1) In this example, the patient has a total of 140 mEq of cation (Na + K) and only 70 mEq of anion (Cl). The remaining 70 mEq (to balance the 140 mEq of cation) must be bicarbonate. (See Schwartz 9th ed., p 54, and Table 3-1.)
TABLE 3-1 Composition of GI secretions
4. Which of the following diagnoses would be most likely in a patient who presents with normovolemic hyponatremia?
A. Syndrome of inappropriate anti-diuretic hormone secretion (SIADH)
B. High output renal failure
C. Water toxicity
D. GI losses
Water toxicity would be associated with hypervolemia. Primary renal disease and GI losses would be expected to result in hypovolemia (Fig. 3-3). A normal volume status in the setting of hyponatremia should prompt an evaluation for a syndrome of inappropriate secretion of ADH. (See Schwartz 9th ed., p 56; See Fig. 3-3A.)
FIG. 3-3A. “ADH = anti-diuretic hormone; SIADH = syndrome of inappropriate secretion of anti-diuretic hormone.”
5. A patient is admitted with a glucose of 500 and a sodium of 151. Which of the following is the best approximation of the patient’s actual serum sodium level?
Hyponatremia also can be seen with an excess of solute relative to free water, such as with untreated hyperglycemia or mannitol administration. Glucose exerts an osmotic force in the extracellular compartment, causing a shift of water from the intracellular to the extracellular space. Hyponatremia therefore can be seen when the effective osmotic pressure of the extracellular compartment is normal or even high. When hyponatremia in the presence of hyperglycemia is being evaluated, the corrected sodium concentration should be calculated as follows: For every 100-mg/dL increment in plasma glucose above normal, the plasma sodium should decrease by 1.6 mEq/L.
For this patient, a serum glucose of 500 is roughly 400 mg above normal. To correct for the elevated serum glucose, multiply 4 × 1.6 = 6.4. This value can be subtracted from 151 to obtain a corrected serum sodium of 144.6. (See Schwartz 9th ed., p 55.)
6. Which of the following is the most likely diagnosis in a patient with a serum sodium of 152 mEq/L, a urine sodium concentration of >20 mEq/L, and a urine osmolality of >300 mOsm/L?
A. Syndrome of inappropriate anti-diuretic hormone (SIADH)
B. Diabetes insipidus
C. Renal tubular disease
D. Cushing’s syndrome
Hypernatremia results from either a loss of free water or a gain of sodium in excess of water. Like hyponatremia, it can be associated with an increased, normal, or decreased extracellular volume (seeFig. 3-3B). Hypervolemic hypernatremia usually is caused either by iatrogenic administration of sodium-containing fluids, including sodium bicarbonate, or mineralocorticoid excess as seen in hyperaldosteronism, Cushing’s syndrome, and congenital adrenal hyperplasia. Urine sodium concentration is typically >20 mEq/L and urine osmolarity is >300 mOsm/L. (See Schwartz 9th ed., p 56.)
This patient has hypernatremia, urinary sodium excretion >20mEq/L and elevated urinary osmolality, which are all suggestive of sodium retention.
FIG. 3-3B. Differential diagnosis of hypernatremia
7. Which of the following can contribute to hyperkalemia in patients with renal insufficiency?
A. Loop diuretics
C. Calcium channel blockers
D. Nonsteroidal anti-inflammatory drugs (NSAIDs)
A number of medications can contribute to hyperkalemia, particularly in the presence of renal insufficiency, including potassium-sparing diuretics, angiotensinconverting enzyme inhibitors, and NSAIDs. (See Schwartz 9th ed., p 56.) Loop diuretics would tend to contribute to hypokalemia. Aspirin and calcium channel blockers have no significant effect on potassium levels.
8. Which of the following would cause decreased deep tendon reflexes?
Hypokalemia causes decreased deep tendon reflexes. Hypomagnesemia and hypocalcemia cause increased deep tendon reflexes. Hypoglycemia has no effect on deep tendon reflexes. (See Schwartz 9thed., p 57.)
9. Which of the following is an early ECG change seen in hyperkalemia?
A. Prolonged PR interval
B. Sine wave formation
C. Peaked T waves
D. Flattened P wave
Although all of the listed findings are associated with hyperkalemia, peaked T waves are the first ECG change seen in most patients.
ECG changes that may be seen with hyperkalemia include high peaked T waves (early), widened QRS complex, flattened P wave, prolonged PR interval (first-degree block), sine wave formation, and ventricular fibrillation. (See Schwartz 9th ed., p 57.)
10. A postoperative patient with a potassium of 2.9 is given 1 mEq/kg replacement with KCl (potassium chloride). Repeat tests after the replacement show the serum K to be 3.0. The most likely diagnosis is
C. Metabolic acidosis
D. Metabolic alkalosis
In cases in which potassium deficiency is due to magnesium depletion, potassium repletion is difficult unless hypomagnesemia is first corrected. (See Schwartz 9th ed., p 57.)
Alkalosis will change serum potassium (a decrease in 0.3 mEq/L for every 0.1 increase in pH above normal). This is not enough to explain the lack of response to repletion in the patient. Metabolic acidosis would not decrease potassium. Calcium does not play a role in potassium metabolism.
11. What is the actual serum calcium level in a patient with an albumin of 2.0 and a serum calcium level of 6.6?
When total serum calcium levels are measured, the albumin concentration must be taken into consideration: Adjust total serum calcium down by 0.8 mg/dL for every 1-g/dL decrease in albumin. (See Schwartz 9th ed., p 57.)
0.8 × 2 = 1.6 + 6.6 = 8.2
12. Which of the following is a cause of acute hypophosphatemia?
A. Chronic ingestion of magnesium containing laxatives
B. Insulin coma
C. Refeeding syndrome
Acute hypophosphatemia is usually caused by an intracellular shift of phosphate in association with respiratory alkalosis, insulin therapy, refeeding syndrome, and hungry bone syndrome. Clinical manifestations of hypophosphatemia usually are absent until levels fall significantly. In general, symptoms are related to adverse effects on the oxygen availability of tissue and to a decrease in high-energy phosphates and can be manifested as cardiac dysfunction or muscle weakness.
Refeeding syndrome occurs when excess calories are given to a starved person (anorexia). Refeeding syndrome is a potentially lethal condition that can occur with rapid and excessive feeding of patients with severe underlying malnutrition due to starvation, alcoholism, delayed nutritional support, anorexia nervosa, or massive weight loss in obese patients. With refeeding, a shift in metabolism from fat to carbohydrate substrate stimulates insulin release, which results in the cellular uptake of electrolytes, particularly phosphate, magnesium, potassium, and calcium. (See Schwartz 9th ed., p 64.)
Magnesium containing laxatives can cause hypermagnesemia in patients with renal failure but does not affect phosphorous levels.
Patients with insulin coma (hypoglycemia) are not at risk for hypophosphatemia. However, hypophosphatemia is common in diabetic ketoacidosis.
Rhabdomyolosis is associated with hyperkalemia and hyperphosphatemia.
13. Hypomagnesemia clinically resembles which of the following?
The magnesium ion is essential for proper function of many enzyme systems. Depletion is characterized by neuromuscular and central nervous system hyperactivity. Symptoms are similar to those of calcium deficiency, including hyperactive reflexes, muscle tremors, tetany, and positive Chvostek’s and Trousseau’s signs (see Table 3-2). Severe deficiencies can lead to delirium and seizures. A number of ECG changes also can occur and include prolonged QT and PR intervals, ST-segment depression, flattening or inversion of P waves, torsades de pointes, and arrhythmias. Hypomagnesemia is important not only because of its direct effects on the nervous system but also because it can produce hypocalcemia and lead to persistent hypokalemia. When hypokalemia or hypocalcemia coexists with hypomagnesemia, magnesium should be aggressively replaced to assist in restoring potassium or calcium homeostasis. (See Schwartz 9th ed., p 58.)
TABLE 3-2 Clinical manifestations of abnormalities in potassium, magnesium, and calcium levels
14. A patient presents obtunded to the ER with the following labs:
Na 130 Cl 105 K 3.2 HCO3 15
Which of the following is the most likely diagnosis?
A. GI losses
B. Lactic acidosis
C. Methanol ingestion
D. Renal failure
This is a normal anion gap acidosis. Lactic acidosis, methanol ingestion, and renal failure are all associated with an increased anion gap. (See Schwartz 9th ed., p 58; See Table 3-3.)
Evaluation of a patient with a low serum bicarbonate level and metabolic acidosis includes determination of the anion gap (AG), an index of unmeasured anions.
AG = (Na) − (Cl + HCO3)
The normal AG is 12 mmol/L and is due primarily to the albumin effect, so that the estimated AG must be adjusted for albumin (hypoalbuminemia reduces the AG). Corrected AG = actual AG − [2.5(4.5 − albumin)].
Metabolic acidosis with an increased AG occurs either from ingestion of exogenous acid such as from ethylene glycol, salicylates, or methanol, or from increased endogenous acid production of the following:
– Hydroxybutyrate and acetoacetate in ketoacidosis
– Lactate in lactic acidosis
– Organic acids in renal insufficiency
TABLE 3-3 Etiology of metabolic acidosis
Increased Anion Gap Metabolic acidosis
Exogenous acid ingestion
Endogenous acid production
Normal Anion Gap
Acid administration (HCl)
Loss of bicarbonate
GI losses (diarrhea, fistulas)
Renal tubular acidosis
Carbonic anhydrase inhibitor
15. Which of the following is the best choice to replace isotonic (serum) fluid loss?
A. D5 ¼ NS with 20 mEq KCl/liter
B. D5 ½ NS with 20 mEq KCl/liter
C. 3% saline solution
D. Lactated Ringer’s
Lactated Ringer’s best approximates serum electrolytes and would be the fluid of choice to replace isotonic serum fluid loss. (See Schwartz 9th ed., p 60; See Table 3-4.)
TABLE 3-4 Electrolyte solutions for parenteral administration
16. Which of the following should be the first treatment administered to a patient with a potassium level of 6.3 and flattened P waves on their ECG?
B. Insulin and glucose
C. Calcium gluconate
D. Inhaled albuterol
Treatment options for symptomatic hyperkalemia are listed in Table 3-5. The goals of therapy include reducing the total body potassium, shifting potassium from the extracellular to the intracellular space, and protecting the cells from the effects of increased potassium. For all patients exogenous sources of potassium should be removed, including potassium supplementation in IV fluids and enteral and parenteral solutions. Potassium can be removed from the body using a cation-exchange resin such as Kayexalate that binds potassium in exchange for sodium. It can be administered either orally, in alert patients, or rectally. Immediate measures also should include attempts to shift potassium intracellularly with glucose and bicarbonate infusion. Nebulized albuterol (10 to 20 mg) may also be used. Use of glucose alone will cause a rise in insulin secretion, but in the acutely ill this response may be blunted, and therefore both glucose and insulin may be necessary. Circulatory overload and hypernatremia may result from the administration of Kayexalate and bicarbonate, so care should be exercised when administering these agents to patients with fragile cardiac function. When ECG changes are present, calcium chloride or calcium gluconate (5 to 10 mL of 10% solution) should be administered immediately to counteract the myocardial effects of hyperkalemia. Calcium infusion should be used cautiously in patients receiving digitalis, because digitalis toxicity may be precipitated. All of the aforementioned measures are temporary, lasting from 1 to approximately 4 hours. Dialysis should be considered in severe hyperkalemia when conservative measures fail. (See Schwartz 9th ed., p 60, and Table 3-5.)
TABLE 3-5 Treatment of symptomatic hyperkalemia
Oral administration is 15–30 g in 50–100 mL of 20% sorbitol
Rectal administration is 50 g in 200 mL of 20% sorbitol
Glucose 1 ampule of D50 and regular insulin 5–10 units IV
Bicarbonate 1 ampule IV
Counteract cardiac effects
Calcium gluconate 5–10 mL of 10% solution
D50 = 50% dextrose.
17. The approximate IV rate for maintenance fluids for a 50-kg patient would be
A. 75 ml/hr
B. 90 ml/hr
C. 105 ml/hr
D. 120 ml/hr
Once the daily total is established, dividing by 24 will give an approximate hourly rate. Alternatively, dividing by 25 (instead of 24) gives a rapid approximate rate. In other words, the hourly IV rate will be
4 ml/kg/hour for the 1st 10 kg
2 ml/kg/hour for the 2nd 10 kg
1 ml/kg/hour for each kg >20 kg
In this example, 4 × 10 = 40 (for the 1st 10 kg), 2 × 10 = 20 (for the 2nd 10 kg), and 1 × 30 = 30 (for the remaining kg). 40 + 20 + 30 = 90 ml/hr. (The number if one divides by 24 instead of 25 is 87.5 ml/hr.) (See Schwartz 9th ed., p 63.)