Chapter 2 Fluid and Electrolyte Management of the Surgical Patient
Principles of Surgery Companion Handbook
FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENT
|Anatomy of Body Fluids|
|Total Body Water|
|Normal Exchange of Fluid and Electrolytes|
|Classification of Body Fluid Changes|
|Fluid and Electrolyte Therapy|
|Preoperative Fluid Therapy|
|Intraoperative Fluid Management|
|Postoperative Fluid Management|
Water constitutes 50 to 70 percent of the total body weight. At 1 year of age, the total body water averages 65 percent of body weight. The figure for the average adult male is 60 percent of body weight, and for adult females, it is 50 percent of body weight.
The water of the body is divided into three functional compartments, intracellular and extracellular, which is further divided into intravascular and interstitial. The intracellular fluid varies between 30 and 40 percent of the body weight because of the body's diverse cell population. The extracellular water represents 20 percent of body weight, with approximately one-third of this being intravascular fluid.
The chemical composition of the intracellular fluid includes potassium and magnesium as the principal cations. Phosphates and proteins are the principal anions. In the extracellular fluid, sodium is the principal cation and chloride and bicarbonate are the principal anions. Because plasma has a higher protein content (organic anions), its concentration of cations is higher and it has fewer inorganic anions than interstitial fluid. In any given solution, the number of milliequivalents of cations present is balanced by precisely the same number of milliequivalents of anions.
The differences in ionic composition between intracellular and extracellular fluid are maintained by the semipermeable cell membrane. Although the total osmotic pressure of a fluid is the sum of the partial pressures contributed by each of the solutes in that fluid, the effective osmotic pressure depends on those substances which fail to pass through the pores of the semipermeable membrane. The dissolved proteins in the plasma are primarily responsible for effective osmotic pressure between the plasma and the interstitial fluid compartments, also known as the oncotic pressure. While sodium, as the principal cation of the extracellular fluid, contributes a major portion of the osmotic pressure, it is the intravascular proteins that do not penetrate the cell membrane freely that constitute the oncotic pressure.
Because cell membranes are completely permeable to water, the effective osmotic pressures in the intracellular and extracellular compartments is maintained by redistribution of water between the compartments. Fluid shifts between the intracellular, intravascular, and interstitial fluid compartments are triggered by changes in the volume, concentration, or composition of the extracellular fluid.
Optimal care of the patient undergoing major surgery requires a working knowledge of the basic principles governing the internal and external exchanges of water and salt. Homeostasis of the body's fluid environment, normally maintained by the kidneys, may be compromised by surgical stress, abnormal hormonal controls, or injuries to the lungs, skin, or gastrointestinal tract.
The normal individual consumes an average of 20002500 mL of water per day, in the form of liquids and solid food. The daily losses average 250 mL in stool, 8001500 mL in urine, and approximately 600 mL as insensible losses through the skin and lungs. The mandatory minimum urine output to excrete nitrogenous wastes is approximately 500 mL/day. Fever increases the insensible losses through the skin. Hyperventilation increases the insensible losses through the lungs.
Daily salt intake varies from 5090 mEq as sodium chloride. The kidneys usually excrete the excess salt. Sweat represents a hypotonic loss of fluids of 1560 mEq/L. Insensible fluid losses from the skin and lungs do not contain salt.
The volume and composition of various gastrointestinal secretions are shown in Table 2-1. Excessive gastrointestinal losses should be replaced by an isotonic salt solution.
TABLE 2-1. COMPOSITION OF GASTROINTESTINAL SECRETIONS
Disorders of fluid balance may be classified in three categories: disturbances of volume, concentration, and composition.
Volume deficit or excess usually is diagnosed by clinical examination of the patient. The blood urea nitrogen (BUN) level rises with an extracellular deficit. The serum creatinine level usually does not increase proportionally in those with healthy kidneys, and this discrepancy often is used to differentiate between prerenal and renal azotemia. The hematocrit increases with extracellular fluid deficit and decreases with an extracellular excess. The serum sodium concentration is not related to the volume status of extracellular fluid; a severe volume deficit may exist with a normal, low, or high serum sodium level.
Volume Deficit Extracellular fluid volume deficit is the most common fluid disorder in the surgical patient. The most common causes include loss of gastrointestinal fluids from vomiting, nasogastric suction, diarrhea, and fistula drainage. Other common causes include sequestration of fluid in soft tissue injuries, infection, tissue inflammation, peritonitis, intestinal obstruction, and burns. Acute, rapid losses result in central nervous system (CNS) and cardiovascular signs, but slower, more insidious losses are well tolerated until severe extracellular volume deficit exists. Thermal regulation may become a problem in the hypovolemic patient, and body temperature actually may vary with environmental temperature. The febrile response to illness may be suppressed in hypovolemic patients. Severe volume depletion depresses all body systems and interferes with clinical evaluation of a patient.
Volume Excess Extracellular fluid volume excess is an iatrogenic condition or may be secondary to renal insufficiency, cirrhosis, or congestive heart failure. In the healthy young adult, the signs of circulatory overload, manifested primarily in the pulmonary circulation, are well tolerated. In the elderly patient, congestive heart failure with pulmonary edema may develop quickly with even a moderate volume excess.
Sodium is the ion primarily responsible for the osmolarity of the extracellular fluid space. Hypo- and hypernatremia can be diagnosed on clinical grounds when the rate of change in extracellular sodium concentration is rapid. Slower changes in concentration should be noted early by laboratory tests and corrected promptly.
Hyponatremia Acute symptomatic hyponatremia is characterized by CNS signs of increased intracranial pressure (ICP). The excessive intracellular water associated with hyponatremia may lead to increased ICP. Oliguric renal failure may develop with severe hyponatremia if replacement of sodium salts is delayed. Hyponatremia is not universally caused by administration of hypotonic solutions. Many hypovolemic conditions result in hyponatremia when sodium loss is in excess of free water losses.
Hypernatremia Acute symptomatic hypernatremia results in CNS and tissue signs except when hypertonic sodium solutions have been administered. Hypernatremia is universally associated with intravascular volume depletion. While volume changes occur frequently without any change in serum sodium concentration, the reverse is not true.
Mixed Volume and Concentration Abnormalities Mixed volume and concentration abnormalities may develop as a consequence of the disease stage or as a result of inappropriate parenteral fluid therapy. One of the more common mixed abnormalities is an extracellular fluid deficit in hyponatremia. This occurs when a patient continues to drink water while losing large volumes of gastrointestinal fluids. In the postoperative period, when gastrointestinal losses are replaced with a hypotonic sodium solution, a similar condition exists.
Normally functioning kidneys can minimize these changes and compensate for many of the imprecise replacements associated with parenteral fluid administration. Patients who have an extracellular volume deficit or who have oliguric or anuric renal failure are prone to develop mixed volume and osmotic concentration abnormalities. Fluid and electrolyte management in these patients therefore must be precise. Mild volume deficits in elderly patients with borderline renal function may result in significant fluid and electrolyte abnormalities. These changes usually are reversible with prompt correction of the extracellular fluid volume deficit.
Disorders of acid-based balance and changes in the concentration of K+, Ca2+, and Mg2+ are common in surgical patients.
Acid-Base Balance The pH of body fluids is usually maintained within narrow limits despite the large load of acid produced as a by-product of cellular metabolism. These acids are neutralized efficiently by several buffering systems and subsequently eliminated by the lungs and the kidneys. The most important buffers include proteins, phosphates, and the bicarbonatecarbonic acid system. The four types of acid-base disturbances include respiratory acidosis and alkalosis and metabolic alkalosis and acidosis. A primary respiratory disturbance may result in a compensatory metabolic change in an attempt to maintain pH homeostasis. A metabolic disturbance often results in a more rapid respiratory compensatory disturbance in a similar fashion. A thorough knowledge of pH, bicarbonate concentration, and PaCO2 allows an accurate diagnosis of most acid-base disturbances. Clinical interpretation must be made in association with the patient's clinical history.
Respiratory Acidosis This condition is associated with retention of CO2 secondary to decreased alveolar ventilation in surgical patients, acute problems resulting in inadequate ventilation including airway obstruction, atelectasis, pneumonia, pleural effusion, pain from an upper abdominal incision, abdominal distention, or excessive use of narcotics. Management involves prompt correction of the pulmonary defect, endotracheal intubation, and mechanical ventilation if necessary. Strict attention to tracheobronchial hygiene in the postoperative period is important.
Respiratory Alkalosis This condition usually is caused by apprehension, pain, hypoxia, CNS injury, and iatrogenic assisted ventilation. In the acute phase, the serum bicarbonate concentration is normal, and the alkalosis develops as a result of a rapid decrease in the PaCO2. The dangers associated with severe respiratory alkalosis are related to hypokalemia and ventricular tachyarrhythmias. Other complications include a disadvantageous shift in the oxyhemoglobin dissociation curve, limiting the ability of hemoglobin to unload oxygen to the tissues. Treatment is directed at correcting the underlying problem, including appropriate sedation, analgesia, proper use of a mechanical ventilator, and correction of preexisting potassium deficits.
Metabolic Acidosis This disorder results from the retention or gain of acids or the loss of bicarbonate. The most common causes include renal failure, diarrhea, small bowel fistula, diabetic ketoacidosis, and lactic acidosis. The initial compensation is an increase in minute ventilation and depression of the PaCO2. Even with normal kidneys, metabolic acidosis may develop when excessive amounts of chloride ion are used in replacement crystalloid solutions. The anion gap is a useful tool in delineating the etiology of metabolic acidosis. The gap is calculated from a sum of serum chloride and bicarbonate levels subtracted from the serum sodium concentration. The anion gap is a laboratory anomaly because routine chemistry tests include Na, K, Cl, and HCO3. The unmeasured anions therefore account for the gap and include sulfate, phosphate, lactate, and other organic anions.
The most common cause of an elevated anion gap is shock or inadequate tissue perfusion resulting in lactic acidosis. Diabetic ketoacidosis, starvation, ethanol intoxication, and poisoning by methanol, ethylene glycol, or excessive amounts of aspirin also produce increased anion gaps. Treatment of the metabolic acidosis should be directed toward correction of the underlying disorder. Bicarbonate therapy should be reserved only for the treatment of severe acidosis and only after the advantages of a compensatory respiratory alkalosis are used. The use of sodium bicarbonate after cardiac arrest should be guided by serial measurements of pH and PaCO2.
Metabolic Alkalosis This disorder results from the loss of fixed acids or the gain of bicarbonate and is aggravated by hypokalemia. The pH and serum bicarbonate concentration are elevated. Respiratory compensation is small and usually not detected. Primary compensation for metabolic alkalosis is usually by renal mechanisms. A common problem in the surgical patient is a hypochloremic, hypokalemic metabolic alkalosis resulting from extracellular volume deficits. Ordinarily, the urinary excretion of bicarbonate increases to compensate for the alkalosis. However, in the volume-depleted patient, aldosterone-mediated sodium resorption results in reabsorption of bicarbonate in an attempt to improve volume status. The removal of bicarbonate from the glomerular filtrate results in a paradoxical aciduria and a self-perpetuating metabolic alkalosis. Prompt management with an isotonic sodium chloride solution and replacement of the usual potassium depletion are indicated. Occasionally, severe metabolic alkalosis with excessive gastrointestinal fluid losses requires the infusion of acidic solutions such as ammonium chloride, arginine hydrochloride, or 0.2 N hydrochloric acid. Correction of the alkalosis should be gradual over a 24-h period with frequent measurements of pH, PaCO2, and serum electrolytes.
Ninety-eight percent of the potassium in the body is located within the intracellular compartment. At a concentration of 150 mEq/L, it is the major cation of intracellular water. The small amount of extracellular potassium is critical to cardiac and neuromuscular function in maintaining transmembrane gradients required for transmission of an electrical impulse. Rapid shifts of potassium into and out of cells are designed to maintain a critical transmembrane gradient and are easily affected by acidosis and cellular injury. When renal function is normal, dangerous hyperkalemia is encountered rarely.
Hyperkalemia Significant hyperkalemia results in cardiovascular signs including bradyarrhythmias, heart blocks, and cardiac arrest. Gastrointestinal symptoms including nausea, vomiting, colic, and diarrhea are associated with disturbances in muscular dysfunction. Treatment includes withholding exogenous potassium, administering intravenous calcium, or administering bicarbonate, glucose, and insulin to promote cellular uptake of potassium. In severe hyperkalemia, enteral administration of cation exchange resins, such as Kayexalate, or hemodialysis is required.
Hypokalemia This is a more common problem in surgical patients. The etiologies include excessive renal excretion, intracellular shift of extracellular potassium, excessive administration of potassium-free parenteral fluids, and losses in gastrointestinal secretions. Chronic potassium losses associated with diuretic use may result in a diminished ability to shift potassium into and out of cells to correct acid-base disorders. Gradual replacement of total body potassium stores is required.
The signs of potassium deficit include cardiac tachyarrhythmias and abnormal contractility of skeletal and smooth muscle and flaccid paralysis. Treatment should be intravenous replacement with no more than 40 mEq/L of intravenous fluid and should not exceed 40 mEq/h.
Most of the 1000 g of calcium in the average-sized adult is found in bone in the form of phosphate and carbonate salts. Normal daily intake is 13 g, most of which is excreted by the gastrointestinal tract. The normal serum level is 8.510.5 mg/dL, half of which is bound to albumin and plasma proteins. The fraction of calcium that is ionized changes in relationship to the pH. Acidosis causes an increase in the ionized fraction.
In the routine postoperative course, disturbances of calcium metabolism are infrequent. In the critically ill patient with large fluid shifts and capillary leak, ionized calcium levels usually are low but unpredictable, and replacement therapy should be guided by serial determinations.
Hypocalcemia The symptoms of hypocalcemia include numb-ness and tingling of the circumoral region and the tips of the fingers and toes. The signs of hypocalcemia include hyperactive tendon reflexes, positive Chvostek's sign, muscle cramps, tetany with carpopedal spasm, seizures, and electrocardiographic (ECG) changes.
The most common causes include acute pancreatitis, massive soft tissue infections, renal failure, pancreatic and small bowel fistulas, and hypoparathyroidism. Transient hypocalcemia is a frequent occurrence after removal of parathyroid adenomas. Hypocalcemia also is associated with severe hypomagnesemia.
Treatment of hypocalcemia is directed toward correcting the underlying cause and repletion. Acute symptoms usually are treated with intravenous calcium chloride or gluconate. Chronic losses may be supplemented orally, with or without vitamin D.
Hypercalcemia The early manifestations of hypercalcemia include fatigue, lassitude, weakness, anorexia, nausea, vomiting, and weight loss. With severe hypercalcemia, lassitude gives way to somnambulism, stupor, and coma. The two major causes of hypercalcemia are hyperparathyroidism and cancer with bony metastases.
A serum calcium concentration of 15 mg/dL or higher requires emergency treatment. Vigorous volume repletion with salt solutions dilutes the calcium level and increases urinary calcium excretion. Once the extracellular volume deficit has been corrected, increased renal clearance can be augmented by furosemide administration.
The use of oral and intravenous inorganic phosphate also lowers the serum calcium level by inhibiting bone resorption. If administered too quickly, intravenous phosphorous can cause an abrupt fall in calcium with the formation of calcium phosphate complexes and may result in tetany, hypotension, and acute renal failure. Intravenous sodium sulfate also lowers the serum calcium level by increasing urinary excretion of calcium.
Corticosteroids decrease resorption of calcium from bone and reduce the intestinal absorption of vitamin D. They are useful in treating hypercalcemic patients with sarcoidosis, myelomas, myolymphomas, and leukemias, although the reduction in serum calcium level may not be apparent for 12 weeks. Mithramycin, a cytotoxic drug, effectively lowers the serum calcium level in 2448 h by direct action on bone. Calcitonin induces a moderate decrease in the serum calcium level, but the effect is diminished with repeated administration. The definitive treatment of acute hypercalcemic crisis in patients with hyperparathyroidism is immediate surgery.
The total body content of magnesium in the average adult is approximately 2000 mEq, about half of which is incorporated in the bone. The distribution of magnesium is similar to that of potassium, primarily intracellular. Serum magnesium concentration normally ranges from 1.52.5 mEq/L. The normal dietary intake of magnesium is approximately 20 mEq. Most is excreted in feces and some in urine.
Magnesium Deficiency Magnesium deficiency occurs with starvation, malabsorption syndromes, large losses of gastrointestinal fluid, large-volume crystalloid resuscitation with magnesium-free solutions, and during total parenteral nutrition with inadequate quantities of magnesium replacement. Other causes include acute pancreatitis, diabetic ketoacidosis, primary aldosteronism, chronic alcoholism, amphotericin B therapy, and a protracted course after thermal injury.
The magnesium ion is essential for proper function of most enzyme systems. The signs and symptoms are similar to those of calcium deficiency. A concomitant calcium deficiency occasionally is noted and is refractory to treatment in the absence of magnesium repletion.
The diagnosis of magnesium deficiency depends on an awareness of the syndrome and occasionally clinical recognition of the symptoms. Laboratory confirmation is available but may not be reliable because the syndrome may exist in the presence of a normal serum magnesium level. The surgical patient who is maintained on parenteral fluids in the long term deserves routine magnesium administration.
Treatment of magnesium deficiency is by parenteral administration of magnesium sulfate or magnesium chloride. With normal renal function, as much as 2 mEq of magnesium per kilogram of body weight per day can be administered in the face of severe depletion. The intravenous route is preferable for initial treatment, and large doses should be administered over a 4-h period. Acute magnesium toxicity should be avoided, and monitoring of vital signs and continuous ECG monitoring should be routine for doses larger than 40 mEq. Calcium chloride or calcium gluconate should be available to counteract any adverse effects of hypermagnesemia.
To replete the intracellular compartment may take 13 weeks, and the asymptomatic patient may require intramuscular or oral replacement with magnesium sulfate or magnesium oxide, respectively.
Magnesium should not be given to the oliguric patient or in the presence of hypovolemia unless actual magnesium depletion has been demonstrated. Considerably smaller doses should be used in the patients with renal insufficiency.
Magnesium Excess Symptomatic hypermagnesemia is rare but usually is seen in patients with severe renal insufficiency. Serum magnesium levels tend to parallel changes in potassium concentration in these patients. Retention and accumulation of magnesium occur in any patient with impaired glomerular or renal tubular function. The problem is compounded with acidosis or when the patient takes magnesium-containing antacids or laxatives. Other causes include early thermal injury, massive trauma, severe extracellular volume deficit, and severe acidosis.
The early signs and symptoms of magnesium excess include lethargy, weakness, and interference with cardiac conduction and resemble those seen in hyperkalemia. Somnolence leading to coma and muscular paralysis occur in the later stages. Treatment consists of replenishing any preexisting extracellular volume deficit, correcting acidosis, and withholding exogenous magnesium. Acute symptoms may be alleviated with intravenous administration of calcium. Peritoneal dialysis or hemodialysis is indicated for chronically elevated levels.
Many different electrolyte solutions, with various compositions, are available for parenteral administration. The choice of a particular fluid depends on the patient's volume status and electrolyte balance.
The ideal isotonic salt solution for replacing gastrointestinal losses and extracellular fluid volume deficits, in the absence of gross abnormalities of concentration and composition, is lactated Ringer's solution. It contains 130 mEq of sodium balanced by 109 mEq of chloride and 28 mEq of lactate. Lactate is readily converted to bicarbonate by the liver and is used instead of bicarbonate because is it more stable in storage. Concern about the ability of the liver to metabolize lactate is unwarranted even when infusing large quantities of lactated Ringer's solution to patients in hemorrhagic shock.
Isotonic sodium chloride is the intravenous fluid best used for initial correction of an extracellular fluid volume deficit in the presence of hypernatremia, hypochloremia, and metabolic alkalosis. It contains 154 mEq of sodium and 154 mEq of chloride per liter. The high concentration of chloride above the normal serum concentration of 103 mEq/L may not be rapidly excreted by the kidneys, and a dilutional acidosis may develop. The kidneys should easily excrete the excess chloride.
In the postoperative period, 0.45% sodium chloride in 5% dextrose solution is used to provide free water for insensible losses and some sodium for renal adjustment of the serum concentration. With added potassium, this is a reasonable solution to use for maintenance requirements in patients with an uncomplicated course requiring only a short period of parenteral fluids.
Preoperative evaluation and correction of existing fluid disorders are an integral part of surgical care. Determination of a particular fluid disorder is facilitated by categorizing the abnormalities as volume, concentration, and compositional changes. Although some disease states produce characteristic changes in fluid balance, each disturbance should be regarded as a separate entity. Volume changes cannot be predicted accurately from a knowledge of the serum sodium level because an extracellular volume deficit or excess may exist with a normal, low, or high sodium concentration. Similarly, any of the four primary acid-based disturbances may be associated with any combination of volume and concentration abnormalities. Close observation and frequent evaluation of the clinical situation are the most rewarding approach.
CORRECTION OF VOLUME CHANGES
Changes in the extracellular fluid volume are the most frequent and important abnormalities encountered in the surgical patient. The diagnosis of volume changes is made almost entirely on clinical grounds. The signs exhibited by an individual patient depend not only on the relative or absolute quantity of extracellular fluid lost but also on the rapidity with which it is lost.
Volume deficits may result from external loss of fluids or from an internal redistribution of extracellular fluid into a nonfunctional compartment. Whereas external losses may be witnessed or easily measured, internal distribution is more difficult to evaluate and quantify. Although the concept of a third space is not new, it is usually considered in patients with massive ascites, burns, or crush injuries. Perhaps more important is the third-space loss into the peritoneum, the bowel wall, and other tissues with inflammatory lesions of the intraabdominal organs. Realizing that the peritoneum has approximately 2 m2 of surface area, the magnitude of these losses may be substantial. Swelling of the bowel wall and mesentery and secretion of fluid into the lumen of the bowel can cause loss of several liters of fluid. Similar deficits may occur with massive infection of the subcutaneous tissues (necrotizing fascitis) or with severe crush injury.
These third-space losses are sometimes referred to as parasitic because they remain part of the extracellular fluid space and equilibrate very slowly. The term nonfunctional is used because the fluid is no longer able to participate in the normal function of the extracellular fluid compartment. The patient with ascites may have an enormous total extracellular fluid volume, but the functional component is severely depleted. This patient will evoke the signs and symptoms of an extracellular fluid volume deficit without changes in weight or obvious compositional changes.
Exact quantification of these deficits is impossible and probably unnecessary. Acute losses of fluid from the extracellular compartment are more likely to result in cardiovascular signs. Gradual or chronic losses are better tolerated but insidious.
Upon diagnosis of a volume deficit, prompt fluid replacement with a balanced salt solution should be initiated. Clinical observation of the reversible signs of the volume deficit and establishment of an hourly urine output of 3050 mL are used as general guidelines indicating the adequacy of resuscitation. Usually a reliable index of volume replacement, the hourly urine output can be misleading. An osmotic diuresis as a result of hyperglycemia in critically ill patients and patients with chronic renal disease may cause inappropriately high urinary volumes. Reliance on a formula or a single clinical sign is perilous in determining when adequate fluid replacement has occurred.
Rate of Fluid Administration The rate of fluid administration varies depending on the severity and type of fluid disturbance, the presence of continuing losses, and the cardiac status of the patient. The most severe volume deficits may be replaced safely with isotonic solution at rates up to 2000 mL/h. Constant observation by the physician is mandatory, and the rate of replacement should be reduced as the fluid status improves. Elderly patients with associated cardiovascular disorders require slower, more careful correction with constant monitoring of the cardiopulmonary system. If urinary output is not restored promptly, measurements of central filling pressures and cardiac output may be required to prevent renal injury from underresuscitation and congestive heart failure from excessive volume restoration.
CORRECTION OF CONCENTRATION CHANGES
If symptomatic hyponatremia or hypernatremia complicates volume loss, prompt correction of the concentration abnormality to relieve symptoms is necessary. Volume replenishment should be accomplished with slower correction of the remaining concentration abnormality. For immediate correction of severe hyponatremia, 5% sodium chloride or molar sodium lactate is used. The sodium deficit is estimated by multiplying the decrease in serum sodium concentration below normal by the total body water. The patient should be reevaluated before complete correction of the concentration disorder. Although most of the sodium is found in extracellular fluid, the estimate is based on total body water because the effective osmotic pressure in the extracellular compartment cannot be increased without proportionately increasing it in the intracellular compartment. In treated moderate hyponatremia with an associated volume deficit, volume replacement can be started immediately with normal saline. Should a concomitant metabolic acidosis exist, M/6 sodium lactate (167 mEq/L each of sodium and lactate) may be used.
Treatment of hyponatremia associated with volume excess is by restriction of water. In the presence of severe symptomatic hyponatremia, a small amount of hypertonic salt solution may be infused initially to alleviate symptoms.
For the correction of severe symptomatic hypernatremia with an associated volume deficit, 5% dextrose in water should be infused until symptoms are relieved. If the correction is too rapid, convulsions and coma may result. Correction of hypernatremia concomitant with repletion of the volume deficit by half-normal saline or half-strength lactated Ringer's solution is safer.
COMPOSITION AND MISCELLANEOUS CONSIDERATIONS
Correction of existing potassium deficits should be started only after an adequate urine output is obtained. Should the patient have a concomitant metabolic alkalosis, less potassium may be required with shifting of the potassium out of the intracellular compartment as the alkalosis is corrected. Calcium and magnesium rarely are needed during preoperative resuscitation but should be given as necessary.
Prevention of volume depletion in the preoperative period is important. Prolonged periods of fluid restriction or the use of cathartics and enemas for preparation of the bowel may cause significant acute losses of extracellular fluid. Recognition and treatment of these losses will minimize complications during the operative period.
If preoperative replacement of extracellular fluid volume has been incomplete, hypotension may develop promptly with the induction of anesthesia. Compensation for a mild volume deficit in the awake patient may be revealed when these compensatory mechanisms are abolished with anesthesia.
In addition to blood losses during operation, there may be extracellular fluid losses during procedures requiring extensive dissection, evaporative losses from the open abdomen or chest, edema of the bowel wall, or collections within the lumen of the bowel and the peritoneal cavity. Replacement of these losses in the form of the balanced salt solution markedly reduces postoperative oliguria. Administration of blood should be used to maintain an acceptable red blood cell mass. The addition of albumin to intraoperative blood and fluid replacement is not necessary and potentially harmful. Balanced crystalloid solutions should be administered at a rate of 0.51 L/h during major abdominal operations, unless there are other measurable losses.
IMMEDIATE POSTOPERATIVE PERIOD
Evaluation of the patient in the recovery room, determination of the amount of fluid lost or gained during the operation, and a review of the preoperative fluid status should precede orders for postoperative fluids. Correction of any existing deficit should be prompt, and maintenance fluids for the remainder of the day should be ordered initially. Frequent assessments of the vital signs and urinary output facilitate appropriate fluid management in the first 24 h after operation.
Postoperative hypotension and tachycardia require prompt investigation and appropriate therapy. Smaller volume deficits are less noticeable, and evaluation of the level of consciousness, pupillary size, breathing patterns, skin warmth and color, body temperature, and urine output are recommended. Operative blood loss usually is underestimated by the operating surgeon by 1540 percent. Serial laboratory studies of the hematocrit, electrolytes, and blood gases may be helpful. Ongoing signs and symptoms of volume deficit, despite adequate volume replacement, should lead one to suspect that there is continuing losses of blood or other extracellular fluids.
LATER POSTOPERATIVE PERIOD
The problem of volume management during the postoperative convalescent phase is one of accurate measurement and replacement of all losses. The measured sensible losses, usually of gastrointestinal origin, should be replaced with an isotonic salt solution. The insensible losses, as a result of increased hypermetabolism, hyperventilation, and fever, should be replaced with 5% dextrose in water. In individuals with normal renal function, the specific crystalloid solution and electrolyte concentration are less important. The determination of serum electrolyte levels in patients with an uncomplicated postoperative course often is unnecessary. A prolonged period of parenteral replacement or excessive losses, either sensible or insensible, or some degree of renal insufficiency warrants daily determinations of serum electrolytes and possibly nutritional supplementation.
SPECIAL CONSIDERATIONS IN THE POSTOPERATIVE PATIENT
Volume Excesses Administration of isotonic salt solutions in excess of volume losses may result in overexpansion of the extracellular fluid space. The kidneys may be able to excrete the additional sodium, but after several days, the signs and symptoms of overload may be noted. The earliest sign of volume overload is weight gain. Edema, tachypnea, and fatigue are early signs of volume overload. Circulatory and pulmonary signs of overload represent a massive overload or even moderate overload in patients without significant cardiopulmonary reserve. Excessive total extracellular fluid with a concomitant depletion of the intravascular circulating volume may coexist and represent a significant challenge in postoperative care.
Hyponatremia When hypotonic solutions are used to replace sensible measured losses, hyponatremia can develop. Insidious hyponatremia can develop if the patient has good kidney function. Excessive losses of sodium through the urine may develop in elderly patients with salt-losing kidneys. Neurologic deficits also may develop. This problem may be avoided by administering isotonic solutions in the early postoperative period.
In the presence of hyperglycemia, pseudohyponatremia may develop. The osmotic effect of glucose in the extracellular compartment may cause the transfer of cellular water into the extracellular compartment, diluting the sodium. This problem may be addressed by correcting the hyperglycemia.
Hypernatremia Hypernatremia is uncommon but dangerous in the postoperative period. Invariably, in the surgical patient, hypernatremia results from excessive water losses. Insensible losses should be replaced with 5% dextrose in water. Occasionally, osmotic diuretics such as mannitol and urea also can result in losses of water in excess of sodium, resulting in hypernatremia. Again, 5% dextrose in water should be used to correct the serum sodium level, and the osmotic diuretics should be discontinued and/or removed by dialysis.
ACUTE RENAL FAILURE
Acute renal insufficiency after trauma or surgical stress is a lethal complication. Acute renal failure is classified according to its cause as prerenal, renal, or postrenal. The most common cause in the postoperative period is shock from volume depletion or cardiac failure. The most common intrarenal causes include endotoxemia, trauma, drugs, and myoglobin. Postrenal causes are mechanical obstruction of the ureter, bladder, or urethra.
Therapy of acute renal failure begins with removal of the cause. Correcting the volume deficit or removing the nephrotoxic agent is mandatory. Postrenal obstructions should be addressed appropriately.
Maintaining homeostasis during acute renal failure involves removing organic acids produced by intermediary metabolism. Additional indications for dialysis include hyperkalemia, azotemia with complications, fluid overload, hyperkalemia, and the need to remove other waste products of metabolism.
Predisposing Factors The most common predisposing factors to renal failure include trauma, sepsis, cardiopulmonary bypass, renal transplantation, urologic surgery, vascular disease, preexisting renal disease, radiographic contrast agents, and drugs. The evaluation of patients with acute renal failure requires urine chemistry and urine hematology, inspection of the urine sediment, and thoughtful analysis of the development of azotemia in relationship to various interventions during the care of the patient.
Management of the Patient with Established Acute Renal Failure Disorders of fluid and electrolytes require initial attention. The oliguric or anuric patient represents a special challenge because the administration of various solutions becomes more important. The use of dialysis is governed by the severity of the electrolyte and fluid disorders exhibited by the patient. The four forms of dialysis for acute renal failure include hemodialysis, peritoneal dialysis, continuous arteriovenous hemodialysis, and continuous venovenous ultrafiltration.
High-Output Renal Failure Uremia occurring without oliguria is a more frequent but less well recognized disorder than acute renal insufficiency. Clinical experience and laboratory experiments suggest that high-output renal failure represents a less severe renal injury than that required to produce oliguric renal failure. The primary danger of high-output renal failure is the delay in recognition because of normal urine output. Inappropriate administration of various medications and potassium can cause significant problems. The disorder usually is self-limiting.
For a more detailed discussion, see Shires GT III, Barber A, and Shires GT: Fluid and Electrolyte Management of the Surgical Patient, chap. 2 in Principles of Surgery, 7th ed.
Copyright © 1998 McGraw-Hill
Seymour I. Schwartz
Principles of Surgery Companion Handbook