AN OVERVIEW OF FLUID AND ELECTROLYTE PROBLEMS IN THE SURGICAL PATIENT

GEORGE G. LIM, MD, FPCS

THE SURGICAL PATIENT DEFINITION ETIOLOGY/ETIOPATHOGENESIS CLINICAL MANIFESTATIONS MANAGEMENT Non-Pharmacologic Pharmacologic LABORATORY/ANCILLARY PROCEDURES FOLLOW -UP/PREVENTION/PREVENTIVE MEASURES/PROPHYLAXIS EXAMPLE CASE PREOPERATIVE ASSESSMENT Patients tolerate operations best when they are properly hydrated. For the majority of patients, this poses no problem, as reflected in the absence of peripheral edema, the presence of normal vital signs, stable weight, adequate urine output, good skin turgor, moist mucous membranes, and normal serum electrolytes. The usual surgical patient therefore, does not need much fluid and electrolyte correction. Preexisting deficits are minimal and insignificant, operative manipulation is kept to a minimum, and early return of oral food intake is expected. This is especially true for almost all elective minor to medium operations and many of the elective major surgical procedures. The dehydrated patient, however, will not tolerate operation as well. He is likely to develop hypotension at the time of induction of anesthesia, which may be further aggravated by the fluid losses encountered during the operation. Similarly, edematous tissues in the patient who is over hydrated are more difficult to dissect, heal less efficiently, and frequently will not hold stitches. Overeagerness to hydrate a patient scheduled for an elective uncomplicated surgical procedure is one common cause of this problem. It is for these reasons that the preoperative fluid and electrolyte status of all patients must be assessed carefully to identify who will require special attention and management prior to undergoing operation. How can Fluid Balance be assessed ?

The usual surgical patient with no preexisting deficit based on the clinical history will have normal vital signs, good skin turgor, moist mucous membranes, adequate urine output, and stable body weight. Serum electrolyte determination may be unnecessary if there are no indications of a major volume or electrolyte abnormality and the contemplated surgical procedure does not entail too much fluid or electrolyte changes. On the other hand, the most common disorder encountered in the preoperative patient is dehydration with accompanying salt loss, also called volume deficit. Pathologic conditions that give rise to this state include intestinal obstruction, diarrhea, various enterocutaneous fistulas, and the sequestration of extracellular fluid in injured tissues. Since exact quantification of these losses is virtually impossible, the degree of volume deficit must be based on a detailed history of the patients disease coupled with a careful evaluation of the physical signs. The history will often reveal the duration and severity of the fluid loss. External losses such as vomiting or diarrhea may be reflected as weight loss. By far, the most common source of these losses is the gastrointestinal tract. As with maintenance needs, proper replacement of these losses can be accomplished if one remembers the basic composition of gastrointestinal secretions and their relation to the composition of normal serum. (Table 1). Internal losses (third space losses), though, are often not appreciated and may reach massive proportions despite minimal weight loss. Nevertheless, other signs may be of value. A patient with sunken eyes, loss of skin turgor, and a dry tongue is much more dehydrated than one without these findings. Of particular importance is an assessment of the cardiovascular status. Depressed blood pressure, rapid pulse, and low urinary output are all indices of significant volume depletion. (Table 2). Accompanying these findings are a hemoconcentrated serum, a urine of high specific gravity, and an elevated blood urea nitrogen. Depending upon the tonicity (osmolality) of the fluid losses, the serum electrolytes may be normal or reflect individual electrolyte abnormalities.

Table 1. Composition of Gastrointestinal Secretions TYPE OF VOLUME Na SECRETION (ml/24hr) mEq/L Saliva 1000-1500 5-10 Stomach 1000-2000 60-90 Pancreas 600-800 135-145 Bile 300-600 135-145 Small Intestine 2000-3000 120-140 Colon 60

K mEq/L 20-30 10-15 5-10 5-10 5-10 30

Cl mEq/L 5-15 100-130 70-90 90-110 90-120 40

HCO3 mEq/L 25-30 95-115 30-40 30-40

Clinically significant volume depletion usually does not become manifest until a loss of fluid approximating 5% of the body weight has occurred. Under these circumstances, skin turgor is usually depressed, eyes may be sunken, mucous membranes have lost their moistness, and urine volume is decreased and
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hyperconcentrated. With severe degrees of volume loss (10% or more), urine volume is markedly depressed, tachycardia is almost always present and may be accompanied by shortness of breath, and blood pressure is quite labile. Based in these observations, a rough approximation of the volume deficit can be made. Thus, a 70 kg male who has lost 5% of his body weight (3.5 kg) will need about 3.5 liters of fluid to restore homeostasis. Table 2. Clinical Manifestations of Volume Deficit Type of Sign Central Nervous System VOLUME DEFICIT

Gastrointestinal System Cardiovascular System

Moderate Sleepiness Apathy Slow responses Anorexia Cessatio of usual activity Progressive decrease in food consumption Orthostatic hypotension Tachycardia Collapsed veins Collapsing pulse Soft, small tongue with longitudinal wrinkling Decreased skin turgor

Tissue

Severe Decreased tension reflexes Anesthesia of distal extremities Stupor Coma Nausea, vomiting Refusal to eat Silent ileus & distention Cutaneous lividity Hypotension Distant heart sounds Cold extremities Absent pulses Atonic muscles Sunken eyes

INTRAOPERATIVE LOSSES What are some of the Losses encountered during Surgery ? A unique fluid loss encountered in the postoperative patient is that brought about by sequestration at the site of operative trauma. This situation is created when interstitial fluid or plasma is sequestered in abnormal amounts in an area of tissue injury. Depending upon the magnitude of the operation, such losses may be small or exceedingly great. The several hundred milliliters of fluid lost in an inguinal hernia repair is generally of no physiologic significance. On the other hand, the extracellular fluid sequestered in a Total Proctocolectomy may be quite substantial. Since there is no way to measure these losses accurately, replacement must, at best, be based upon clinical approximation. Evaporation of water from exposed viscera is another source of fluid loss. This depends to a large extent on the duration and magnitude of the operative procedure. Replacement is again based upon clinical approximation. Another source of volume loss at surgery is blood. This can generally be estimated by measuring accurately the amount of blood suctioned out of the operative

site and the blood remaining at the sponges. Weighing the used blood-soaked gauze and then subtracting the weight of the dry unused gauze from this is a useful method of approximating intraoperative blood loss. Since estimation of fluid losses is based to a large extent on clinical approximation, volume replacement is done using primarily the urine output, the vital signs, particularly the pulse rate, and the central venous pressure, if available. Some arbitrary but clinically useful guidelines are as follows: (1) Blood should be replaced to maintain an acceptable red blood cell mass irrespective of any additional fluid and electrolyte therapy. (2) The replacement of extracellular fluid should begin during the operative procedure. (3) Balanced salt solution needed during operation is approximately 0.5 to 1 L/h, but only to a maximum of 2 to 3 L during a 4-h major abdominal procedure, unless there are other measurable losses. MAINTENANCE REQUIREMENTS Regardless of the patients disease or type of operative procedure performed, water and salt losses occur daily through normal urinary output and evaporative losses from the skin and lungs. These normal maintenance requirements consist of both sensible and insensible losses depending upon whether they can be measured readily. Usually, 500 to 750 ml of a balanced salt solution is added to the maintenance requirements for the first two or three postoperative days to compensate for these losses plus the fluid sequestered at the operative site. Thereafter, the sequestered fluid will return to the intravascular compartment once normal capillary function to the affected area is restored. What are the Sensible and Insensible Losses of Water ? Insensible losses (those not visible or not readily measurable) occur from water losses through the lungs and evaporative losses from the skin. They usually amount to about 600-1000 ml daily in the non-active and non-perspiring adult. Sensible losses (those that are visible and readily measurable) include water losses in the feces and those due to excretion of urine. In the absence of diarrhea, water loss via the feces is essentially negligible and can be ignored. Urinary losses vary considerably depending upon the state of ones hydration, but generally a volume of water approaching 10001500 ml is required to excrete the daily solute load of the adult surgical patient in a urine concentration isoosmotic with plasma. Depending upon the patients age, sex, weight, and body surface areas, daily maintenance requirements for both sensible and insensible losses will approach 15002500 ml. Since the electrolyte composition of these losses is low (particularly in the first 48-72 hours following operation), adequate replacement can be supplied under most circumstances with a 5% Dextrose and water solution. A rule of thumb that has been useful in estimating these needs is to multiply the patients weight in kilograms times 30 ml per kg. A 70 kg male, therefore, would need approximately 2100 ml of water daily to meet normal maintenance requirements. What are the Normal Daily Electrolyte Requirements ?
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Although urine and insensible losses are primarily water losses, it must remembered that each of these sources contains sodium, potassium, and chloride, albeit in small amounts. For the patient requiring intravenous therapy for only short periods of time, replacement of these electrolytes is unimportant. In the individual requiring parenteral support for several days to a week or more, total body stores of these ions will eventually diminish if some replacement is not provided. This is particularly important for sodium, since a depletion of this ion can initiate an extracellular hypotonicity, resulting in a shift of water intracellularly and a state of water intoxication. Since exact determination of these electrolyte losses is neither practical nor necessary on a daily basis, replacement should be based on the usual requirements of most patients. For sodium, daily needs range from 50-125 mEq, while for potassium and chloride, they approach 40-100 mEq. For practical purposes, however, usual replacement requirements for each of these ions is approximately 60-70 mEq daily. In meeting this needs, a second rule of thumb that can be used is to provide one mEq of these electrolytes for each kilogram of body weight. In a patient requiring 2 liters of fluid to meet normal maintenance requirements, 1500 ml can be provided as dextrose and water, and the remaining 500 ml can be given as saline with the addition of potassium chloride in appropriate quantities. POSTOPERATIVE FLUID MAINTENANCE PROBLEMS What are the Usual Postoperative Fluid Problems ? Volume Overload: Causes, Manifestations, and Treatment A wide variety of fluid disorders may occur in the postoperative period, but by far , the most common clinical problem observed at this time is volume overload. Characterized by an isotonic expansion of the extracellular fluid compartment, this condition occurs when fluid having the same tonicity as plasma (such as balance salt solutions, including normal saline and Ringers Lactate solution) are infused intravenously in excess of body needs. Such solution do not affect the osmolality of the extracellular space; hence, no net shifts in water between this compartment and the intracellular space occurs. Therefore, intracellular volume remains unchanged, and any excess fluid infusion is reflected as an increase in the volume of the extracellular compartment alone. The greater the excess infusion, the greater will be the expansion of this compartment with a corresponding decrease in the concentration of hemoglobin, hematocrit, and protein, even though the concentration of sodium remains unchanged. This complication can occur at any time postoperatively, but it is particularly common in the early postoperative period when the hormonal response of the patient having undergone the stress of operation is one that results in maximal retention of water and sodium. There is no physiologic evidence to support the hypothesis that an hourly urine volume of 100 ml is any better than 50 ml unless there is some concurrent pathologic renal process contributing to the overall clinical situation. The misconception that excess salt water will be excreted by the kidneys automatically if the body has no
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use for it is fallacious. It is the change in tonicity of the extracellular fluid space that allows the kidney to retain or excrete water and electrolytes. As long as urinary output of 30-50 ml per hour is maintained, renal perfusion will be adequate, and renal failure is most unlikely. The earliest sign of fluid overload is increase in body weight. This is a particularly important sign in the postoperative patient, since the normal catabolic processes during postoperative recovery and convalescence usually results in a weight loss of 1/4 to 1/2 pound per day. Depending upon the extent of fluid expansion, peripheral edema may be present. This clinical situation is usually accompanied by an increase in central venous pressure, a high pulse pressure, swollen eyelids, hoarseness, and occasionally exertional dyspnea. If this is unrecognized and uncorrected, pulmonary edema may ensue with signs of frank dyspnea, coughing, distended neck veins, and crackles on the lungs upon auscultation. When detected early, volume restriction, which consists of withholding all fluids until excess water and electrolytes have been excreted, may restore balance. Usually though, diuretic supplements will be necessary. If cardiac reserve is compromised, digitalis must also be given. For most purposes, furosemide which inhibit renal tubular reabsorption of sodium and water, will prove entirely satisfactory. Except in unusual circumstances, low doses (10-25 mg) given as single IV doses are sufficient if normal renal function has been maintained. In the presence of severe renal impairment, some form of dialysis may be needed to resolve the problem. Accurate hemodynamic monitoring cannot be overemphasized to prevent over treatment. Volume Deficit: Causes, Manifestations, and Treatment Volume deficit is another problem encountered postoperatively, though not as common as volume overload. This usually results from gastrointestinal losses due to nasogastric suction, enterostomies, enterocutaneous fistulas, and diarrhea or sequestered losses that occur at the operative site. Like volume overload, volume depletion primarily affects the extracellular fluid compartment since losses are generally isoosmotic with plasma. As plasma volume decreases, interstitial fluid slowly moves into the vascular space to support the depleted circulation, resulting in an overall deficit in the volume of the extravascular extracellular fluid compartment (interstitial fluid compartment). The clinical manifestations of volume depletion include weight loss, tachycardia, weak pulse, dry mucous membranes, and if sufficiently severe, hypotension, particularly of the orthostatic variety. Some degree of oliguria is almost always present. If urinary sodium is measured, it is frequently below 10 mEq/L owing to the action of aldosterone on the renal tubules. A rise in the hematocrit and hemoglobin is frequently also present, due to hemoconcentration, since the red cell mass is unchanged. Because losses are isoosmotic with plasma, there is usually no change in the serum sodium concentration. Because renal perfusion is diminished, the urine becomes hyperconcentrated (specific gravity greater than 1.020), and some elevation of the blood urea nitrogen (BUN) and creatinine is almost always present.

The treatment of volume depletion will depend to a large extent on the composition of the fluid lost. In most instances, replacement with a balanced salt solution will prove satisfactory. If large amounts of proteins have been lost, plasma or an albumin-containing fluid should be administered in conjunction with the balanced salt solution. Because of the difficulty in assessing the degree of volume deficit, the best guide to follow is adequacy of the hourly urinary output. In the absence of underlying renal disease, glycosuria, or diuretic administration, a urine volume of 30-50 ml per hour with a specific gravity of 1.015 or less suggests satisfactory repletion of volume deficits. Reversion of hemoglobin and hematocrit levels may also be helpful, though not as reliable. Composition Problems: Hyponatremia With the emphasis in the recent years on giving adequate volumes of isotonic salt solutions both intraoperatively and postoperatively to maintain circulatory stability and adequate urinary output, deficits in serum sodium concentration are not commonly encountered. If hyponatremia should occur, it usually develops in the early postoperative period when water retention is maximal secondary to the stress of operation. The underlying pathophysiology of this condition is the abnormal expansion of all body fluids owing to excess water. In contrast to excess infusion of salt solution in which volume increases but tonicity of the extracellular compartment remains unchanged, water alone not only increases the volume of this compartment but correspondingly decreases the concentration of the extracellular ions. The resulting hypotonicity of the extracellular space relative to the tonicity of the intracellular compartment causes a net diffusion of water into the cells until both compartments are isoosmotic. Thus, an increase in volume occurs in both the extracellular and intracellular compartments at the expense of a decrease in ionic concentrations. Hyponatremia then ensues even though the total body content of sodium may be normal or even increased. Three clinical situations may give rise to hyponatremia. The first is the inappropriate replacement of body salt losses by infusing water alone or dextrose-water alone. Hyponatremia may also occur in the patient with head injury or preexisting renal disease. The hyponatremia associated with head injury is probably due to the inappropriate secretion of anti-diuretic hormone with excessive water retention, while the defect in the patient with renal disease is due to a renal tubular dysfunction resulting in an inability to concentrate urine appropriately. Finally, hyponatremia may occur from one of two metabolic processes: the water of oxidation from utilization of nutrient fuel and mobilization of water from cellular catabolism. Approximately 750 gm of tissue is catabolized daily following a major operation and thereby could produce 500 ml of endogenous water. The detrimental aspect of hyponatremia is not the low sodium per se but the volume increase in the intracellular fluid compartment. As water moves intracellularly, cells begin to swell. For most cells, this poses no major problem, but when brain cells swell, an increase in intracranial pressure will eventually ensue since the brain is

enclosed in a fixed space within the skull. Clinically, the patient may have the following manifestations: confusion, apathy, weakness, nausea, vomiting, muscle twitching, convulsions, stupor, coma or eventually death. Treatment is directed primarily toward restricting water intake which in most instances may be all that is necessary. In cases where hyponatremia is severe, this may not be enough and efforts should be employed to raise the serum sodium concentration to at least 130 mEq/L. Correction using normal saline infusion should be deliberate, cautious, and absolutely without haste. Composition Problems: Hypernatremia When hypernatremia occurs, it is always accompanied by a decrease in the volume of the intracellular compartment owing to the increased osmolality of the extracellular space, which tends to draw water from cells until an isoosmotic equilibrium has been established between the two compartments. A variety of disorders may give rise to this condition, but particularly common in the postoperative period is fever in the septic patient. Several liters of salt-free water may be lost daily through evaporation of sweat. Patients with tracheostomies may also lose water through insensible loss. Patients with renal disease or those who sustain injuries to the central nervous system or who have undergone intracranial surgery are also at high risk. In both situations, extremely large volumes of solute-poor urine may be excreted daily. Solute loading, for whatever reason, may also give rise to hypernatremia. Tube feeding, if not diluted with enough water, may precipitate a tremendous extracellular water diuresis. A similar condition may develop if hypertonic saline is infused too rapidly to replace massive sodium losses or to promote the excretion of excess body fluids. Diabetic patients may develop hypernatremia from nonketotic hyperosmolar dehydration secondary to the diuresis from hyperglycemia and glycosuria. The clinical manifestations often develop insidiously. Some thirst is usually present. Irritability and restlessness are common. Disorientation, convulsions, stupor, and coma may also develop in severe cases. Owing to the dire consequences of this problem, every effort must be made to correct this condition. Correction of the underlying cause should be made immediately. To correct the hypertonicity, adequate volumes of water as 5% glucose solution intravenously or by mouth should be administered to restore electrolyte concentrations to normal and maintain adequate urine volumes. In most instances, one to two days of fluid administration will be required before the serum sodium concentration returns to normal. Composition Problems: Potassium Abnormalities Potassium is usually unnecessary and may prove detrimental if given during the first 24 hours following surgery. Endogenous release of intracellular potassium from tissue catabolism, operative trauma, or blood transfusion, if given, generally provides sufficient quantities of this ion to warrant restriction during the early postoperative period.

However, in contrast to sodium metabolism, in which a variety of exquisite neurohormonal and renal mechanisms are initiated postoperatively to maintain normal body stores, the kidney continues to excrete large amounts of potassium (30-60 mEq per L) daily even beyond the first 24 hours. This continues even if there is inadequate replacement. It is not surprising, therefore, that the most common potassium abnormality encountered during the postoperative period is hypokalemia. In most instances, this deficiency results from either the prolonged administration of potassiumfree IV solutions or the inappropriate replacement of daily potassium losses, particularly those resulting from gastrointestinal losses. Patients with potassium deficiencies commonly exhibit neuromuscular and cardiac disturbances. Symptoms may range from mild muscular weakness and paresthesia to flaccid states. Cardiac manifestations may appear as hypotension, bradycardia, or cardiac arrhythmia. Electrocardiographic changes usually appear as ST segment changes. Of special importance is the danger of digitalis toxicity in patients taking this medication. Once this is diagnosed, care must be taken in correcting the problem since aggressive compensatory therapy always risks creating a hyperkalemia. It is important to ensure that renal function is adequate before administering potassium. Correction of this abnormality is rarely an emergency and a duration of 24-48 hour period of administering the ion is preferred. If possible, oral therapy is the desired approach, using enteric coated potassium chloride tablets and/or potassium-rich foods. If intravenous therapy is needed, KCl should be used. The rate of administration is determined by the existing potassium deficit, but in most instances, should not exceed 150-200 mEq per day or 10-15 mEq per hour. During the replacement, continuous electrocardiographic monitoring and frequent potassium determinations are mandatory. Once the estimated deficit has been corrected and the serum potassium has returned to normal, maintenance replacement can be resumed. In contrast to hypokalemia, hyperkalemia is distinctly uncommon in the postoperative period and usually indicates some degree of renal impairment. As with hypokalemia, the detrimental effect of elevated serum potassium levels is on myocardial function and may result in bradycardia, hypotension, ventricular fibrillation, and cardiac arrest. Characteristic electrocardiographic manifestations include peaked T waves, depressed ST segments, prolonged PR intervals, diminished P waves, and widened QRS complexes. In contrast to hypokalemia which is seldom an emergency, hyperkalemia, particularly when the serum potassium level is greater than 7 mEq per L, may prove fatal if not corrected rapidly. Treatment includes abrupt cessation of all potassium intake with simultaneous correction of the underlying cause/s. If the potassium level is dangerously high, emergency measures may become necessary to correct it. An intravenous infusion of hypertonic dextrose (50 ml of a 50% dextrose over 30 minutes) together with regular insulin (10-25 units) will lower the extracellular potassium temporarily by promoting its intracellular transport. If acidosis is a contributing factor, the infusion of sodium bicarbonate will rapidly lower the serum potassium level. Since calcium counteracts the toxic effects of hyperkalemia on the heart, the IV infusion of calcium gluconate (5-10 ml of a 10% calcium gluconate solution) over two minutes may also prove very helpful. However, if the patient is receiving digitalis, calcium should not

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be given, as the combination of the two may instead accentuate the toxic effects of hyperkalemia. A long term means of controlling hyperkalemia is to administer a cation exchange resin orally or by enema. The resin binds potassium in the intestine in exchange for sodium. Combined with sorbitol, it enhances the rate of potassium excretion by inducing osmotic diarrhea. Although these measures may initially prove satisfactory, some form of dialysis may ultimately become necessary if the hyperkalemia is due to renal failure. ACID-BASE DISORDERS What are the Usual Peri-operative Acid-Base Disorders ? Acidosis Acidosis is the most important acid-base disorder encountered in the postoperative period because of the potentially devastating effects that acidosis may have on the cardiovascular system. At least three distinct effects have been identified and these include (1) decreased myocardial contractility causing a reduction in cardiac output, (2) decreased responsiveness of the peripheral vasculature to circulating catecholamines, which cause systemic hypotension, and (3) increased refractoriness of the fibrillating myocardium to defibrillation, making efforts at cardiac resuscitation unusually difficult. Although acidosis occurs in response to a wide variety of etiologic factors, the most common postoperative causes include pulmonary insufficiency, poor tissue perfusion leading to lactic acidosis, impairment of renal function, diabetes mellitus, and loss of alkali via gastrointestinal secretions. Regardless of the magnitude of the operation, every effort should be made to ensure satisfactory postoperative ventilation. Any factor that predisposes to depression of the ventilatory effort must be corrected. Attention to tracheobronchial hygiene is mandatory. Deep breathing and coughing, suction of retained tracheobronchial secretions, humidification of air to prevent inspissation of secretions, and the avoidance of oversedation are all important measures to ensure adequate ventilation. Respiratory acidosis is often difficult to diagnose. The common signs are irritability, twitching, hypertension, and tachycardia. Patients who become hypercapneic while breathing room air are always hypoxic, while those who are hypercapneic while receiving supplementary oxygen may have relatively normal arterial oxygen levels. The treatment of respiratory acidosis consists of measures to improve alveolar ventilation In severe cases where pulmonary physiotherapy is inadequate, mechanical ventilatory support may be instituted. A variety of metabolic disorders may also lead to metabolic acidosis. Uncorrected diabetes mellitus may lead to ketoacidosis with a severe extracellular fluid deficit. Renal impairment may lead to retention of nitrogenous waste products, water, and inorganic acids with hyperkalemia and fluid overload. If restriction of potassium and fluids are inadequate, then some form of dialysis may be necessary. Another cause of metabolic acidosis is loss of alkali from the GI tract such as in diarrhea, small bowel obstruction, prolonged drainage of gastrointestinal-cutaneous
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fistulas. Correction of the appropriate fluid and electrolyte abnormalities leads to better correction of the acid-base disorder. Lactic acidosis due to circulatory failure is another cause of metabolic acidosis. Improvement of the hemodynamic abnormality through adequate fluid resuscitation frequently leads also to partial correction of the acidosis. Severe acidosis may be further corrected with infusion of sodium bicarbonate. Alkalosis In contrast to the potentially lethal effects of acidosis, alkalosis is usually well tolerated and is, in fact, the most common acid-base abnormality encountered in the postoperative period. This trend towards alkalosis results from the interaction of one or more of the 4 etiologic components frequently present following operation. Posttraumatic aldosteronism, stimulated by volume reduction during operation, tends to produce extracellular alkalosis through renal inhibition of bicarbonate excretion and excessive excretion of potassium. Nasogastric suction, frequently required to manage the ileus accompanying operation, adds to this alkalotic state by removing hydrogen ions. When large quantities of blood are transfused, the infused citrate is oxidized to bicarbonate, which further favors alkalosis. Finally, hyperventilation secondary to apprehension, pain, or respiratory therapy is frequently present postoperatively and is the most common cause of alkalosis. In most instances, the mild respiratory alkalosis following operation is of trivial importance and requires no specific therapy. Care must be taken to prevent severe hypocapnia especially in patients with compromised cerebral perfusion, and those taking digitalis because of the hypokalemia that may result from the shift of potassium intracellularly. Alkalosis resulting from metabolic disorders, such as over-administration of buffering agents or massive blood transfusion do not pose particular problems since they are corrected spontaneously if renal function is normal. The loss of gastric juice is a different matter. The development of hypochloremic, hypokalemic metabolic alkalosis is self-perpetuating unless the appropriate ions are replaced in adequate amounts. Depending upon the serum electrolyte determination results, sodium, potassium, and chloride must be replaced using normal or half-normal saline with potassium chloride incorporation. Lactated Ringers solution is not to be used since an excess of bicarbonate (lactate or citrate is metabolically converted to bicarbonate) is already present in patients with this syndrome. FLUID AND ELECTROLYTE PROBLEMS BY SPECIFIC CONDITIONS INTESTINAL OBSTRUCTION What are the Metabolic Problems associated with Gastric Outlet Obstruction ? Vomiting or nasogastric suction of gastric juice results in loss of hydrogen ions. The resulting chloride deficit and alkalosis are not easily corrected by the kidneys since
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the hormonally dependent sodium retention and increased renal potassium excretion override the ability of the kidneys to excrete bicarbonate and retain hydrogen ions and restore acid-base equilibrium. As gastric losses continue, the kidneys attempt to maintain intravascular volume and osmolality by further increasing the tubular reabsorption of sodium. This results in excretion of potassium in the urine, promoting more efficient reabsorption of sodium, but compounding the loss of potassium already incurred by vomiting and nasogastric suctioning. Since bicarbonate is reabsorbed with the sodium, the existing alkalosis is further aggravated. As gastric losses continue, and volume loss become more pronounced, sodium reabsorption by the kidneys become virtually complete as does bicarbonate reabsorption. In an attempt to neutralize the alkaline blood, potassium moves intracellularly in exchange for hydrogen ions. This, coupled with the persistent loss of potassium in the urine, results in a severe extracellular depletion of this ion. To conserve whatever potassium is left, the kidneys now reabsorb sodium in exchange for hydrogen ions rather than potassium ions. Not only does this further aggravate the alkalotic state but it also results in a paradoxically acid urine often seen in patients with prolonged metabolic alkalosis. This sequence of events leads to a condition referred to as hypochloremic, hypokalemic metabolic alkalosis. What are the Fluid and Electrolyte Problems encountered in Small Bowel Obstruction ? Accumulation of large quantities of fluid and gas within the lumen of the bowel above an obstruction is striking and progressive. The net movement of a substance across the intestinal mucosa is equal to the difference between the unidirectional flux from the intestinal lumen to blood (absorption) and the opposite flux from blood to lumen (secretion). Accumulation of fluid within the bowel - a negative net flux - will result if the flux from lumen to blood (absorption) is decreased or if the flux from blood to lumen (secretion) is increased. After 48 hours of obstruction, the rate of entry of water into the lumen increases as a consequence of blood to lumen flux. The findings for sodium and potassium is parallel. In an obstructed ileal segment, fluxes from lumen to blood are either decreased or abolished. As a result, water, sodium, and chloride (including possibly other ions) move into the obstructed intestinal segment but not out of it, distending it with fluid having approximately the electrolyte composition as plasma. From experimental data, it appears that the primary cause of fluid loss is increased secretion rather than decreased absorption. When obstruction has been present for a long time, the proximal segments also become involved and gradually distend, losing their ability to handle fluid and electrolytes. A second route of fluid and electrolyte loss is into the wall of the involved intestine, accounting for the boggy, edematous appearance of the bowel. Some of this fluid exude from the serosal surface of the intestinal wall, resulting in free peritoneal fluid. A third route of fluid and electrolyte loss is the most obvious - by vomiting or by nasogastric suction or drainage. The sum of all these fluid losses account for the tremendous fluid and electrolyte abnormality which occurs in an obstructed patient.

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Since the type of fluid that is sequestered is essentially plasma-like in composition, replacement is done using isotonic fluid solutions. The amount of fluid necessary to restore homeostasis is difficult to quantitate and assessment will have to be done using clinical parameters. PERITONITIS What are the Fluid and Electrolyte changes that occur in Peritonitis ? The peritoneum reacts to irritation by vascular dilatation and an outpouring of plasma-like fluid from the extracellular, intravascular, and interstitial compartments into the peritoneal space as an exudate. The loose connective tissue beneath the mesothelium of the viscera, the mesenteries, and the parietes traps extracellular fluid as edema. The atonic, dilated bowel also accumulates fluid in its lumen that is derived from the extracellular fluid volume. This translocation of water, electrolytes, and protein into a sequestered "third space" functionally removes this volume temporarily from the body economy. The rate of functional extracellular fluid loss is proportional to the surface area of peritoneum involved in the inflammatory process. With extensive peritonitis, fluid translocation of 4-6 liters or more in 24 hours is not uncommon. The result is hypovolemia with an isotonic fluid volume deficit. How is the Fluid and Electrolyte abnormality in Peritonitis managed ? Management of this problem necessitates restoration of the intravascular volume with large volumes of fluid to maintain a satisfactory urine output. Since it is difficult to estimate the extent of peritonitis, careful monitoring of the response to fluid resuscitation is necessary, particularly if large fluid volumes are required to maintain an adequate circulation. Monitoring usually entails frequent vital signs, hourly urine output, central venous pressure measurement, or, preferably, Swan-Ganz catheter placement for pulmonary capillary wedge and pulmonary artery pressure determinations. Along with the clinical examination, these measurements provide a good assessment of the adequacy of fluid replacement therapy. There is general agreement that the fluid deficit in patients with peritonitis should be replaced with a crystalloid solution, preferably Ringers lactate although some authors may advocate the addition of colloids. BURNS How is Fluid Loss estimated in Burn Patients ? Cardiovascular alterations occur almost immediately following burn injury. There is a massive shift of fluid and electrolytes from the intravascular and extracellular fluid space into the cells. Reversion of water and sodium from the intracellular fluid space back into the extracellular space begins between the 24th and 48 th hour but is not complete until the tenth post-burn day. In general, these changes are directly
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proportional to the extent and depth of burn. Therefore, any consideration of fluid resuscitation to prevent hypovolemic shock requires an accurate estimation of the magnitude of the burn injury. The burned wound is three-dimensional; therefore, not only the depth but the surface area involved must be estimated. The length and width of the burn wound is expressed as a percentage of the total body surface area displaying either 2nd or 3rd degree burns. The extent is most commonly estimated using the summation of the "rule of nines" (Table 3). Table 3. Rule of Nines for Estimating the Extent of Body Surface Area Burnt. ANATOMIC AREA PERCENT OF BODY SURFACE AREA Head 9 Right Upper 9 Extremity Left Upper Extremity 9 Right Lower 18 Extremity Left Lower Extremity 18 Anterior Trunk 18 Posterior Trunk 18 Neck 1 How is Fluid Resuscitation achieved in Burn Patients ? Although controversy still remains over the solution for resuscitation in burn shock, scientific investigation supports the need for both crystalloid and colloid solutions. It is of little consequence which formula is utilized to begin therapy, as long as this is modified according to the patients changing needs. The Parkland formula, which is the most popular and widely accepted, calls for the administration of 4 ml of lactated Ringers solution per kilogram body weight per percent of body surface area burned during the first 24 hours post-injury. Fluid therapy during the second 24 hours, according to the formula, consists in the administration of free water (Dextrose 5% in water) in quantities sufficient to maintain serum sodium concentration at 140 mEq/L and plasma sufficient to return the plasma volume to normal and sustain adequate perfusion of peripheral organs and tissues. Supplemental potassium is usually not required during the first few days of management. During the first 24 hours, the rate of fluid administration is adjusted to correspond as closely as possible with the rate of extracellular fluid loss. Studies have confirmed that extracellular deficits occur rapidly within the first 6 to 12 hour post-injury. Therefore, one-half of the total calculated volume is delivered during the first 8 hours from the time of injury and the remaining fluids more slowly over the next 16 hours.

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REFERENCES Curreri PW and Luterman A. Burns. In Schwartz, SI (ed): Principles of Surgery, 5th ed. New York, McGraw-Hill Book Co., 1988; 69-104. Kinney JM, and Moore FD. Surgical metabolism in metabolism of body fluids. In Bland, J.H. (ed): Clinical Metabolism of Body Water and Electrolytes. Philadelphia, W.B. Saunders Co., 1963; 337-359. Maxwell MH, Kleeman CR, Narins RG (eds): Clinical Disorders of Fluid and Electrolyte Metabolism, 5th ed. New York, McGraw-Hill,1994 Moore FD, Olesen KH, McMurrey JD, Parker HV, Ball MR, and Boyden CM. Body cell mass and its supporting environment: body composition in health and disease. Philadelphia, W.B. Saunders Co., 1963. Randall HT. Fluid and electrolyte and acid-base balance. Surg Clin North Am, 1976; 56:1019. Shires GT, Canizaro PC, Shires GT III, and Lowry SF . Fluid, electrolyte and nutritional management of the surgical patient. In Schwartz SI (ed): Principles of Surgery, 7th ed. New York, McGraw-Hill Book Co., 1999; 69-104. Skillman JJ. Disturbances of body fluids, ions, and acid-base balance. In Skillman JJ (ed): Intensive Care. Boston, Little, Brown, and Co., 1975; 63-127. Smithline N, and Gardner KD. Gaps - Anionic and Osmolal. J Am Med Asso, 1976; 236:1594 Schwartz SI. Manifestations of gastrointestinal disease. In Schwartz, SI (ed): Principles of Surgery, 5th ed. New York, McGraw-Hill Book Co., 1988; 69-104. Walker AP, and Condon RE. Peritonitis and intraabdominal abscesses. In Schwartz, SI (ed): Principles of Surgery, 5th ed. New York, McGraw-Hill Book Co., 1988; 69-104.

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