Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient

Home , Fluid balance, Water intoxication

4 Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient

Stephen F. Lowry

Objectives

1. To understand the normal electrolyte composition of body fluids and how they are modified by injury and surgical disease. 2. To understand the importance of evaluating fluid status. 3. To recognize the clinical manifestation of common electrolyte abnormalities and methods for their correction. 4. To understand the common manifestation of acid–base abnormalities.

Cases

Case 1 A 72-year-old man undergoes subtotal colectomy for massive lower GI bleeding. He receives ﬁve units of blood during and following operation and is NPO for 6 days while receiving dextrose 5% in water (D5/W) at a rate of 125mL/hour. Urine output remains normal with speciﬁc gravity of 1.012. On the sixth postoperative day, he is disori- ented and combative. Among the results of workup are serum sodium = 119mEq/L, potassium = 3.6mEq/L, chloride = 85mEq/L, glucose = 120mg/dL, blood urea nitrogen (BUN) = 24.

Case 2 A 40-year-old woman presents with a 1 week history of persistent upper abdominal pain in association with nausea and vomiting. She tolerates only small amounts of clear ﬂuids by mouth. No diarrhea is present. Physical examination is unrevealing except for loss of skin turgor and reduced breath sounds over the right chest. Lab re-

sults include sodium = 138mEq/L, potassium = 2.6mEq/L, HCO3 =

62 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 63

43mEq/L. A blood gas is obtained, revealing pH = 7.57, Pao2 = 98mm Hg, Paco2 = 52mmHg, base excess = 10.

Case 3 A 58-year-old woman presents with a 1-week history of confusion, lethargy, and persistent nausea. She has new complaints of back and hip pain. Past history includes a mastectomy for breast cancer 5 years previously. Laboratory values obtained during evaluation include hematocrit (Hct) = 41, white blood count (WBC) = 9000, platelets = 110,000, sodium = 137mEq/L, potassium = 3.8mEq/L, BUN = 25mg/dL, albumin = 3.4g/dL, bilirubin = 1.5g/dL, alkaline phos- phatase = 350IU/L, calcium = 14.2mg/dL.

Introduction

An understanding of changes in ﬂuid, electrolyte, and acid–base concepts is fundamental to the care of surgical patients. These changes can range from mild, readily correctable deviations to life-threatening abnormalities that demand immediate attention. This chapter outlines some of the physiologic mechanisms that initiate such imbalances and methods to systematically evaluate the diverse clinical and biochemi- cal data that lead to decisions regarding therapy. The information and data presented below are intended for application in adult patients, although the principles espoused also are germane to pediatric patients.

Basic Concepts

The Stress Response The normal physiologic response to injury or operation produces a neuroendocrine response that preserves cellular function and pro- motes maintenance of circulating volume. This is readily demon- strable in terms of retention of water and sodium and the excretion of potassium. Many stimuli can produce this response, including many associated with trauma or operation. Activation of several endocrine response pathways increases the levels of antidiuretic hormone (ADH), aldosterone, angiotensin II, cortisol, and catecholamines. Hyperosmo- larity and hypovolemia are the principal stimulants for ADH release, which increases renal water resorption from the collecting ducts and raises urine osmolarity. Aldosterone, the principal stimulus for renal potassium excretion, also is increased by angiotensin II, which can increase both renal sodium and water retention. Aldosterone also is increased by elevated levels of potassium, a common consequence of tissue injury. Hydrocortisone and catecholamine release also contribute to the excretion of potassium. 64 S.F. Lowry

Body Fluid Compartments Total body water (TBW) approximates 60% of body weight (BW) and is divided among the intracellular volume (ICV) as 40% of BW and an extracellular volume (ECV) representing 20% of BW. The ECV is divided further into an interstitial ﬂuid volume (IFV) pool, which is roughly 15% of BW, and the intravascular or plasma volume (PV), which approximates 5% of BW. The TBW is the solvent for most of the solutes in the body, and it is assumed that water moves freely between the ECV and ICV in an effort to equalize the concentration of solutes within each space. However, the solute and colloid concentrations of the ICV and ECV differ markedly. The ECV contains most of the body sodium, while the predominant ICV cation is potassium. Albumin rep- resents the dominant osmotically active colloid within the ECV and virtually is excluded from the ICV. The exogenous administration of electrolytes results in the distribution of that ion to the usual ﬂuid com- partment of highest preferential concentration.

Electrolytes When an electrolyte dissolves in water, it releases positive and negative ions. Although, as noted above, their concentrations vary between ﬂuid compartments, the distribution of water across ﬂuid compartments seeks to equalize the concentration of total solutes and other osmotically active particles. When considering electrolyte problems, it is useful to use the milliequivalent (mEq) measure of their chemical combining capacity. In some cases, this must be converted from the weight expression milligram (mg) expressed on the laboratory report. Table 4.1 assists in this conversion. A millimole (mM) is the atomic weight of a substance expressed in milligrams. A milliosmole (mOsm) is a measure of the number of osmotically active particles in solution. Since mOsm does not depend on valence, the mM dissolved in solution will be the same as mOsm. The osmolarity of a solution depends on the number of active particles per unit of volume (mOsm/L). The normal osmolarity of serum is 290 ± 10mOsm/L. The effective osmolarity (tonicity) involves the mea-

Table 4.1. Data for serum electrolytes. Normal Electrolyte mg/dL mEq/L Sodium 322 140 Potassium 17.5 4.5 Calcium 10 5 Magnesium 2.4 2 Chloride 35.7 102 Phosphorus 3.4 2.0 Source: Reprinted from Pemberton LB, Pemberton DK. Treatment of Water, Electrolyte, and Acid-Base Disorders in the Surgical Patient. New York: McGraw Hill, 1994. With permission of The McGraw-Hill Companies. 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 65 surement of two solutes, sodium and glucose, that represent nearly 90% of ECV osmolarity. This can be modiﬁed by addition of urea concentration, especially in conditions of uremia. The formula for calcu- lating approximate osmolarity is: POSM = 2 ¥ plasma [Na+] + [glucose]/20 + [BUN]/3 Because water moves freely between ﬂuid compartments, ECV osmolarity (or tonicity) is equivalent to that in the ICV.

Maintenance Requirements

There are several principles that underlie the prescription for replacing ﬂuid and electrolytes in surgical patients. This includes a knowledge of normal maintenance requirements as well as replacement for losses.

Water The normal losses of water include sensible (measurable) losses from urine (500–1500mL/day) and feces (100–200mL/day), as well as insensible (unmeasurable) loses from sweat and respiration (8– 12mL/kg/day). Cutaneous insensible losses increase by approximately 10% for each degree C above normal. A method to roughly calculate daily normal water requirements is shown in Figure 4.1. The water of biologic oxidation (catabolism) contributes up to 300mL/day and can be subtracted from these calculations. For healthy adults, an estimated daily maintenance ﬂuid requirement approximates 30 to 35mL/kg/day.

Sodium Sodium losses in urine can vary widely but, in general, approximate daily intake. The normal kidney can conserve sodium to a minimum level of 5 to 10mEq/L. A ﬁgure of 70 to 100mEq Na/day is a reason- able estimate of maintenance level.

Potassium The normal excretion of potassium approximates 40 to 60mEq/day. Since the renal conservation of potassium is not as efﬁcient as for sodium, this is the minimum level of daily replacement in healthy adults (0.5–1.0mEq/kg/day).

Summary of Normal Maintenance Fluids for Surgical Patients In the absence of other comorbidities or prolonged injury/operation induced stress, the NPO surgical patient is adequately maintained by infusion of variable combinations of dextrose (D5) and saline (up to 0.5 N) containing solutions, with approximately 15 to 20mEq/L of potassium added. The rate of infusion should be adjusted to achieve water replacement as outlined above. Such parenteral solutions, when 66 S.F. Lowry

Total Body Water [60% Body Wt. (42L)]

INTRACELLULAR EXTRACELLUAR [40% Body Wt. (28L)] [20% Body Wt. (14L)]

CATIONS CATIONS Na+ 12.0 mEq/L Ca2+ 4.0 mEq/L Na+ 14.2 mEq/L Ca2+ 2.5 mEq/L K+ 150 mEq/L Mg2+ 34.0 mEq/L K+ 4.3 mEq/L Mg2+ 1.1 mEq/L

ANIONS ANIONS Cl– 4.0 mEq/L Proteins 54 mEq/L Cl– 104.0 mEq/L Proteins 14 mEq/L – – HCO3 12.0 mEq/L Other 90 mEq/L HCO3 24 mEq/L Other 5.9 mEq/L 2– – 2– – HPO4 , H2PO4 40 mEq/L HPO4 , H2PO4 2.0 mEq/L

INTERSTITIAL PLASMA (10.5 L) (3.5 L)

Figure 4.1. Distribution of body water and electrolytes in a healthy 70-kg male. (Adapted from Narins RG, Krishna GC. Disorders of water balance. In: Stein JH, ed. Internal Medicine, 2nd ed. Philadelphia: Lippincott Williams & Wilkins. Reprinted from Nathens AB, Maier RV. Perioperative Fluids and Elec- trolytes. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.)

given at an appropriate rate of infusion, sufﬁce to manage the majority of postoperative patients.

Perioperative Fluid and Electrolyte Requirements

The management of fluid and electrolytes in the stressed surgical patient requires a systematic approach to the changing dynamics and demands of the patient. Consideration of existing maintenance requirements, deficits or excesses, and ongoing losses requires regular monitoring and flexibility in prescribing. While the majority of patients require only minor, if any, adjustments in parenteral fluid intake, some present challenging and life-threatening situations.

Fluid Sequestration Following injury or operation, the extravasation of intravascular ﬂuid into the interstitium leads to tissue edema (“third space”). Estimates of this volume for general surgery patients range from 4 to 8mL/kg/h and this volume may persist for up to 24 hours or longer. This loss of functional ECV must be considered as an additional ongoing loss in the early postoperative or injury period. 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 67

Gastrointestinal Losses Additional ongoing losses from intestinal drains, stomas, tubes, and ﬁstulas also must be documented and replaced. The ﬂuid volume and electrolyte concentration of such losses vary by site and should be recorded carefully. Replacement of such losses should approximate the known, or measured, concentration of electrolytes (Table 4.2).

Intraoperative Losses Careful attention to the operative record for replacement of fluids during surgery always is warranted. Usually, additional fluids for prolonged operations and for operations upon open cavities is warranted. Surgeons must know what fluids and medications were given during the procedure so that they can write appropriate postoperative fluid orders. Orders for intravenous fluids may need to be rewritten frequently to maintain normal heart rate, urine output (0.5–1.0mL/kg/h), and blood pressure.

Deﬁning Problems of Fluid and Electrolyte Imbalance

Fluid balance and electrolyte disorders can be classified into distur- bances of (1) extracellular fluid volume; (2) sodium concentration; and (3) composition (acid–base balance and other electrolytes). When confronted with an existing problem of fluid or electrolyte derangement, it is helpful initially to analyze the issues of fluid (water) and electrolyte imbalance separately.

Fluid Status The initial issue is whether a deﬁcit or excess of water exists. A deﬁ- ciency of extracellular volume can be diagnosed clinically (Table 4.3). Acutely, there may be no changes in serum sodium, whereas repeated studies may demonstrate changes in sodium as well as in BUN.

Table 4.2. Volume and composition of gastrointestinal fluid losses. + - + - + Volume Na Cl K HCO3 H Source (mL) (mEq/L) (mEq/L) (mEq/L) (mEq/L) (mEq/L) Stomach 1000–4200 20–120 130 10–15 — 30–100 Duodenum 100–2000 110 115 15 10 — Ileum 1000–3000 80–150 60–100 10 30–50 — Colon 500–1700 120 90 25 45 — (diarrhea) Bile 500–1000 140 100 5 25 — Pancreas 500–1000 140 30 5 115 — Source: Reprinted from Nathens AB, Maier RV. Perioperative fluids and electrolytes. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evi- dence. New York: Springer-Verlag, 2001, with permission. 68 S.F. Lowry Vomiting Diarrhea hwartz SI, ed. Principles of Surgery, sound Functional murmurs Bounding pulse High pulse pressure Increased pulmonary second Gallop Silent ileus and distention and small bowel mesentery Absent peripheral pulses Loud heart sounds activity in food consumption Refusal to eat Edema of stomach, colon, lesser and greater omenta, with longitudinalwrinkling temperature Sunken eyes(97°–99°R) temperature Basilar rales (95°–98°R) Moist rales Symptoms of deficit Symptoms of excess Slow responsesAnorexiaCessation of usual Coma extremities Stupor TachycardiaCollapsed veinsCollapsing pulse Distant heart sounds Cold extremities Hypotension veins Increased cardiac output Distention of peripheral Decreased skin turgor Reprinted from Shires GT, Shires GT III, Lowry S. Fluid, electrolyte and nutritional management of the surgical patient. In: Sc and nutritional management of the surgical GT III, Lowry S. Fluid, electrolyte Shires GT, Shires Reprinted from rectal. system Apathy Anesthesia of distal = Table 4.3.Table Extracellular fluid volume. of SignType Central nervous Moderate SleepinessGastrointestinal Progressive decrease Decreased tension reflexes Severe Nausea, vomiting None At operation: Moderate None Source: Severe Cardiovascular Orthostatic hypotension Cutaneous lividity Elevated venous pressure Pulmonary edema permission of The McGraw-Hill Companies. McGraw-Hill, 1994. With York: 6th ed. New R TissueMetabolic Soft small tongue Mild decrease in Atonic muscles Marked decrease in Subcutaneous pitting edema None Anasarca None 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 69

Under chronic conditions, an assessment of ECV also may be deter- mined from serum sodium level and osmolarity. A high serum sodium (>145mEq/L) indicates a water deficit, whereas low serum sodium (<135mEq/L) confirms water excess. The sodium level provides no information about the body sodium content, merely the relative amounts of free water and sodium. If serum osmolarity is high, it is important to consider the influence of other osmotically active particles, including glucose. Elevated glucose should be treated and will restore, at least partially, serum osmolarity.

Water Excess Although water excess may coexist with either sodium excess or deﬁcit, the most common postoperative variant, hypo-osmolar hyponatremia, may develop slowly with minimal symptoms. Rapid development results in neurologic symptoms that may eventuate in convulsions and coma if not properly addressed as discussed in Case 1. A serum sodium less than 125mEq/L demands immediate attention. Other causes of hyponatremia are listed in Table 4.4. (See Algorithm 4.1 for treatment.) The treatment of water excess involves removing the excess water, adding sodium, or using both approaches to increase serum osmolarity. Restriction of water intake often sufﬁces in that continued sensible and insensible losses will assure free water loss. (The amount of excess water may be estimated by: BW in kg ¥ 0.04 = L of water excess.) In cases in which sodium administration is necessary (i.e., symptomatic

Table 4.4. Causes of hyponatremia. Pseudohyponatremia (normal plasma osmolarity) Hyperlipidemia, hyperproteinemia Dilutional hyponatremia (increased plasma osmolarity) Hyperglycemia, mannitol True hyponatremia (reduced plasma osmolarity) Reduction in ECF volume Plasma, GI, skin, or renal losses (diuretics) Expanded ECF volume Congestive heart failure Hypoproteinemic states (cirrhosis, nephrotic syndrome, malnutrition) Normal ECF volume SIADH Pulmonary or CNS lesions Endocrine disorders (hypothyroidism, hypoadrenalism) Drugs (e.g., morphine, tricyclic antidepressants, cloﬁbrate, antineoplastic agents, chlorpropamide, aminophylline, in- domethacin) Miscellaneous (pain, nausea) SIADH, syndrome of inappropriate antidiuretic hormone secretion. Source: Reprinted from Nathens AB, Maier RV. Perioperative ﬂuids and electrolytes. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evi- dence. New York: Springer-Verlag, 2001, with permission. 70 S.F. Lowry

Patient is hyponatremic Patient is hypernatremic

Rule out artifacts (e.g., from Assess volume status. Monitor presence of glucose, mannitol, cardiovascular, renal, and or glycine). Suspect renal neurologic function. dysfunction and acid–base disorders. Initiate continuous cardiovascular, renal, and neurologic monitoring. Assess volume status. Volume is low

Replace volume deficit with isotonic saline or Volume is low lactated Ringer’s solution.

Correct volume deficit: • Administer isotonic saline if patient is alkalotic. Volume is normal • Administer lactated Ringer’s solution if patient is acidotic. Volume is increased

Give diuretics. Volume is normal

Volume is increased Replace water deficit (no Consider administration more than half in first of a loop diuretic. 24 hr; remainder over 1–2 days). Discontinue infusion when symptoms improve. If neurogenic diabetes insipidus is Evaluate severity of symptoms, present, administer including CNS alterations, vasopressin. hypotension, and oliguria.

Symptoms are mild Symptoms are severe

Restrict water intake. Infuse hypertonic (3%) saline. Do not raise serum sodium by more than 12 mEq/L in first 24 hr. Discontinue infusion when symptoms improve.

Algorithm 4.1. Initial assessment of patient with ﬂuid and electrolyte imbalance. (Reprinted from Van Zee KJ, Lowry SF. Life-threatening electrolyte abnormalities. In: Wilmore DW, Cheung LY, Harken AH, et al, eds. ACS Surgery: Principles and Practice (Section 1: Resuscitation). New York: WebMD Corporation, 1997.) 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 71 hyponatremia), a rise in serum sodium may be achieved by administration of the desired increase of sodium (in mEq/L) = 0.6 (% of BW as TBW) ¥ BW (in kg). An uncommon but devastating complication of raising serum sodium too rapidly is central pontine demyelinating syndrome. This may occur if sodium is increased at a rate >0.5mEq/L per hour. To prevent this complication, it is generally recommended that symptomatic patients receive one half of the calculated sodium dose (using hypertonic sodium solutions, such as 3% saline) over 8 hours to bring serum sodium into an acceptable range (120–125mEq/L), as would be appropriate in Case 1. The remaining dose then may be infused over the next 16 hours. Do not use hypotonic saline solutions until the serum sodium is in an acceptable range. Medications that antagonize ADH effect, such as demeclocycline (300–600mg b.i.d.), also may be used cautiously, especially in patients with renal failure.

Water Excess Caused by SIADH The syndrome of inappropriate ADH (SIADH) results from increased ADH secretion in the face of hypo-osmolarity and normal blood volume. The criteria for this diagnosis also include a reduced aldosterone level with urine sodium >20mEq/L, serum< urine osmolarity, and the absence of renal failure, hypotension, or edema. The syndrome of inappropriate ADH results from several diseases, including malignant tumors, central nervous system (CNS) diseases, pulmonary disorders, medications, and severe stress. The primary treatments for SIADH are management of the underlying condition and water restriction (<1000mL/day). Administration of hypotonic ﬂuids should be avoided.

Water Deficit A deficit of ECV is the most frequently encountered derangement of fluid balance in surgical patients. It may occur from shed blood, loss of gastrointestinal fluids, diarrhea, fistulous drainage, or inadequate replacement of insensible losses. More subtle are “third-space” losses (e.g., peritonitis) or sequestration of fluids intraluminally and intra- murally (e.g., bowel obstruction). Similar to changes in conditions of water excess, a severe or rapidly developing deficit of water may cause several symptoms (Table 4.3). Lab tests for serum sodium (>145mEq/L) and osmolarity (>300mOsm/L) establish the diagnosis. Water deficit results from loss of hypotonic body fluids without adequate replacement or intake of hypertonic fluids without adequate sodium excretion. Patients with decreased mental status or those unable to regulate their water intake are prone to this problem. Patients who are NPO, cannot swallow, or are receiving water-restricted (hypertonic) nutritional regimens also develop this disorder. Excess water loss may result from insensible sources (lungs, sweat) or from excessive gastrointestinal (GI) or renal losses. Large renal losses of hypotonic urine are referred to as diabetes insipidus (DI), which may be of central origin (lack of ADH secretion) or renal (reduces concentrating ability). The most common cause of central DI is trauma. This form often is reversible. Other causes include infections and tumors of the pituitary 72 S.F. Lowry

region. Nephrogenic DI refers to a renal inability to concentrate urine and can be caused by hypercalcemia, hypokalemia, as well as drugs such as lithium. Once a diagnosis of water deficit is entertained, evaluation of urine concentrations can be useful. While water deficit may be associated with either sodium excess or deficit (see Algorithm 4.1), the specific treatment of water deficit must include the administration of free water as a dextrose solution (D5W). Treatment must be done urgently for serum sodium levels >160mEq/L. Up to 1L of D5W may be given over 2 to 4 hours to correct the hypernatremia.

Sodium Concentration Changes As noted earlier, the sodium cation is responsible primarily for main- taining the osmotic integrity of ECV. The signs and symptoms of hyponatremia and hypernatremia can be detected clinically (Table 4.5), especially if changes occur rapidly. More commonly, these changes occur over several days, as noted above. Under such circumstances, mixed volume and concentration abnormalities often occur. Conse- quently, it is important that volume status is assessed initially before any conclusion as to changes in concentration or composition is ascribed.

Sodium Excess In surgical patients, this condition is caused primarily by excess sodium intake (as may occur with infusion of isotonic saline) and renal retention. The proximal signal for these events is a stress response to injury or operation. Chronic sodium excess usually results in edema and weight gain. Classic vascular signs of expanded ECV or frank heart failure may occur, especially in patients with diseases prone to causing edema [congestive heart failure (CHF), cirrhosis, nephrotic syndrome]. Treatment of sodium excess includes eliminating or reducing sodium intake, mobilization of edema fluid for renal excretion (such as osmotic diuretics for fluid and solute diuretics for sodium), and treatment of any underlying disease that enhances sodium retention. An algorithm for assessment of fluid status and acute sodium changes is shown in Algorithm 4.1. Sodium Deficit In the surgical patient, this condition usually occurs via loss of sodium without adequate saline replacement. Several additional sources of sodium loss should be considered, including gastrointestinal fluids and skin. Third-space losses of sodium (and water) also can be extensive after major injury or operation. The symptoms and signs of sodium deficit arise from hypovolemia and reduced tissue perfu- sion. Under such circumstances, urine sodium is low (<15mEq/L) and osmolarity is increased (>450mOsm/L). Prerenal azotemia may be evident (serum BUN/creatinine ratio >20:1). Loss of skin turgor also may occur. Treatment of sodium deficit is directed toward correction of the sodium and water contraction of the ECV. If hypotension is present, this must be treated with normal saline or lactated Ringer’s 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 73 hwartz SI, ed. Principles of Surgery, Flushed skin phase) (decompensated phase) Hyperactive tendon reflexesIncreased intracranial pressure (compensated Increased intracranial pressure to increased intracranial pressurevolume excess) Loss of reflexes Hypotension (if severe) Weakness Maniacal behavior Red, swollen tongue “Fingerprinting” of skin (sign intracellular Dry and sticky mucous membranes Reprinted from Shires GT, Shires GT III, Lowry S. Fluid, electrolyte and nutritional management of the surgical patient. In: Sc and nutritional management of the surgical GT III, Lowry S. Fluid, electrolyte Shires GT, Shires Reprinted from system Muscle twitching Convulsions Restlessness Delirium 6th ed. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies. McGraw-Hill, 1994. With York: 6th ed. New RenalMetabolic None Oliguria that progresses to anuria Oliguria Fever Cardiovascular Changes in blood pressure and pulse secondary Tachycardia Tissue Salivation, lacrimation, watery diarrhea Decreased saliva and tears Table 4.5.Table Consequences of abnormal sodium concentration. of signType Central nervous Moderate: Hyponatremia (water intoxication)Source: Severe: Hypernatremia (water deficit) Moderate: Severe: 74 S.F. Lowry

Table 4.6. Composition of parenteral ﬂuids (Electrolyte Content, mEq/L). Anions Cations Osmolality Solutions Na K Ca Mg Cl HCO3 (mOsm) Extracellular ﬂuid 142 4 5 3 103 27 280–310 Ringer’s lactate 130 4 3 — 109 28* 273 0.9% sodium chloride 154 — — — 154 — 308 D5 45% sodium 77 — — — 77 — 407 chloride D5 W — — — — — — 253 M/6 sodium lactate 167 — -1 — — 167* 334 3% sodium chloride 513 — — — 513 — 1026 Source: Reprinted from Borzotta AP. Nutritional support. In: Polk HC Jr, Gardner B, Stone HH, eds. Basic Surgery, 5th ed. St. Louis: Quality Medical Publishing Inc., 1995.

solution. A mild sodium deficit without symptoms may be treated over several days if the losses of sodium have been reduced. Administration of fluids for water and sodium requires knowledge of the current fluid and electrolyte status of the patient, understanding of the level of stress, and appreciation for actual or potential sources of ongoing fluid and electrolyte losses. Having estimated the fluid and sodium status of the patient, administration of appropriate volumes of water and sodium usually is done by the intravenous route. Standard solutions of known contents nearly always are used, and the prescribing physician must be familiar with these basic formulas (Table 4.6). Abnormalities of other electrolytes (K, Ca, P, Mg: see Abnormalities of Electrolytes, below) usually require specific fluid solutions or addition of these ions to standard solutions. Changes in acid–base balance also may require special alkalotic or acidotic solutions to correct these abnormalities (Tables 4.7 and 4.8).

Table 4.7. Alkalinizing solutions.* Electrolytes total mEq

Solution Tonicity %Solution Volume Na HCO3

NaHCO3 Isotonic 1.5 1L 180 180 NaHCO3 Hypertonic 7.5 50mL 45 45 NaHCO3 Hypertonic 8.3 50mL 50 50 Na lactate Isotonic 1.9 1L 167 167 1/6 molar NaHCO3 Hypertonic 5.0 500mL 300 300 * Some IV alkalinizing solutions are provided with their tonicity, concentration, volume,

and mEq of Na and HCO3. The liver converts each mEq of Na lactate of 1mEq of NaHCO3.

3.75g of NaHCO3 contains 45mEq of NA and 45mEq of HCO3. Solution 1 is made by

taking 800mL of 5% D/W and adding four ampules of 50mL (200mL) of 7.5% NaHCO3.

Also, one or more 50-mL ampules of 7.5 NaHCO3 (No. 2) can be added to 1 lL of 5% D/W or /2 N saline and will provide 1amp. = 45, 2amps. = 90, and 3amps. =

135mEq of Na and HCO3 to the IV solution. Source: Reprinted from Pemberton LB, Pemberton DK. Treatment of Water, Electrolyte, and Acid-Base Disorders in the Surgical Patient. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies. 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 75

TABLE 4.8. Acidifying solutions.* Electrolytes total mEq

Solution Tonicity Percent Volume NH4 C1

NH4 C1 Hypertonic 26.75 20mL 100 100 NH4 C1 Hypertonic 2.14 1L 400 400 HC1 Isotonic 0.1N 1L 100 100 * Acidifying solutions that can be used to treat metabolic alkalosis. These solutions would be used only if KC1 and NaC1 IV solutions were unable to correct the alkalosis. Source: Reprinted from Pemberton LB, Pemberton DK. Treatment of Water, Electrolyte, and Acid-Base Disorders in the Surgical Patient. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies.

Disorders of Composition By deﬁnition, composition changes include alterations in acid–base balance plus changes in concentration of potassium, calcium, magnesium, and phosphate. Acid–Base Balance There are four major buffers in the body: proteins, hemoglobin, phosphate, and bicarbonate. All serve to maintain the hydrogen ion concentration within a physiologic range. Bicarbonate is by far the largest of these buffer pools and follows the equation:

+ H + HCO3 ´ H2CO3 ´ H2O + CO2

This buffer system involves regulation of CO2 by the lungs and HCO3 by the kidneys. Changes in CO2 are reflected as Paco2 in arterial blood gases. Respiratory acid–base abnormalities are identified readily by determination of Paco2. By contrast, there are no definitive means to identify a “metabolic” acid–base abnormality. Two approaches have been used. The first is the concept of anion gap, which is used to identify a nonvolatile or fixed acid–base abnormality. Given that many blood anions are not measured routinely, the difference between the measured cations and anions is called the “anion gap” [Anion gap =

Na - (HCO3 + Cl)]. The normal value is 12. Metabolic acidosis is the most common reason for increases with accumulation of anions such as lactate, acetoacetate, sulfates, and phosphates. (Note: hyper- chloremic acidosis may occur without an anion gap.) The second approach involves measurements of base excess and base deficit. Base excess measures the amount of nonvolatile acid loss or extra base that has increased the total buffer base. Base deficit measures the amount of lost base or extra acid that has decreased the buffer base. The normal value is 0 ± 2.5mEq/L. Base excess (>2.5mEq/L) rep- resents metabolic alkalosis, whereas base deficit (<-2.5mEq/L) repre- sents metabolic acidosis. The four types of acid–base abnormalities are shown in Table 4.9. • Respiratory acidosis results from hypoventilation with retention of

CO2. This frequently occurs in postoperative patients who have received heavy sedation or have been extubated prematurely. 76 S.F. Lowry increased ammonia formation formation Chloride shift into red cells hwartz SI, ed. Principles of Surgery, 1 20 20:1 Excretion of bicarbonate, 20:1 Increased rate and depth 20:1 Increased rate and depth of 20:1 Retention of bicarbonate = > < > < 3 23 Denominator Renal Denominator Renal Numerator Pulmonary (rapid) Numerator Pulmonary (rapid) HCO BHCO ≠ Ø Ø ≠ ventilation, encephalitis decreased ammonia fistulasbicarbonate respiratory acidosis respiratory alkalosis Depression of respiratory Hyperventilation: Diarrhea, small bowelDiuretics Renal (slow) as in 2 2 loss of base lactic acid accumulation, ratio or (decreased alveolarventilation) center: morphine, CNS(increased alveolarventilation) injury ratio Emotional distress,acids severe pain, assisted ratio Excretion of acid salts, retention of acid salts, bicarbonatebicarbonate starvation obstruction of breathing breathing Gain of base Potassium depletion Excessive intake of suction with pyloric ratio Renal (slow) as in Reprinted from Shires GT, Shires GT III, Lowry S. Fluid, electrolyte and nutritional management of the surgical patient. In: Sc and nutritional management of the surgical GT III, Lowry S. Fluid, electrolyte Shires GT, Shires Reprinted from 6th ed. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies. McGraw-Hill, 1994. With York: 6th ed. New Table 4.9.Table Commonly encountered acid-base disorders. of acid–base Type disorderRespiratory acidosis Retention of CO Defect Common causesCNS, central nervous system. Source: Compensation Respiratory alkalosis Excessive loss of CO Metabolic acidosis Retention of fixed Diabetes, azotemia, Metabolic alkalosis Loss of fixed acids or gastric Vomiting 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 77

• Respiratory alkalosis results from hyperventilation leading to

depressed arterial levels of CO2. It may occur in patients experienc- ing pain or those undergoing excessive mechanical ventilation. Alka- losis causes a shift in the oxyhemoglobin-dissociation curve that can lead to tissue hypoxia. Respiratory alkalosis also can lead to reduced levels of potassium and calcium. • Metabolic acidosis results from the overproduction of acid (lactate, ketoacidosis) and also may result from excessive loss of bicarbonate from diarrhea or bowel fistulas. • Metabolic alkalosis is caused by loss of fixed acid or bicarbonate retention. As discussed in Case 2, a classic example is loss of acid- rich gastric juice via nasogastric tubes. Usually, there is an associated ECV depletion. Total body potassium and magnesium deficits mandate judicious replacement. Occasionally, 0.1N hydrochloric acid infusions are needed to reverse the alkalosis. Regardless of whether the initial acid–base disorder is metabolic or respiratory, a secondary compensatory response occurs within the other system. The changes associated with acute and compensated acid–base disorders are shown in Table 4.10. This opposes the pH abnormality and seeks to restore balance. The adequacy of that compensatory response may be impaired by a variety of associated conditions or medications. If the pH value is in the same direction as the respiratory diagnosis (low pH and elevated Paco2), then the respiratory problem is primary. Opposing changes in pH and Paco2 suggest a primary metabolic diagnosis.

Abnormalities of Electrolytes Potassium: Only about 2% of total body potassium is located in the ECV. Nevertheless, slight alterations in plasma potassium may dra- matically alter muscle and nerve function. As a consequence, abnormalities of potassium concentration require expeditious treatment.

Table 4.10. Respiratory and metabolic components of acid–base disorders. Acute (Uncompensated) Chronic (partially compensated) Plasma Plasma - - PCO2 HCO3 *PCO2 HCO3 * Type of acid–base (respiratory (metabolic (respiratory (metabolic disorder pH component) component) pH component) component) Respiratory acidosis ØØ ≠≠ N Ø≠≠≠ Respiratory alkalosis ≠≠ ØØ N ≠ØØØ Metabolic acidosis ØØ N ØØ Ø Ø Ø Metabolic alkalosis ≠≠ N ≠≠ ≠ ≠? ≠

* Measured as levels of standard bicarbonate, whole blood buffer base, CO2 content, or CO2 combining power. The base excess value is positive when the standard bicarbonate level is above normal and negative when the standard bicarbonate level is below normal. Source: Reprinted from Shires GT, Shires GT III, Lowry S. Fluid, electrolyte and nutritional management of the surgical patient. In: Schwartz SI, ed. Principles of Surgery, 6th ed. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies. 78 S.F. Lowry

Hyperkalemia (>6mEq/L) requires immediate intervention to prevent refractory cardiac arrhythmias. Sudden increases in potassium level usually are caused by infusion or increased transcellular flux resulting from tissue injury or acidosis. More chronic elevations of potassium suggest an impairment of renal excretion. Algorithm 4.2 addresses treatment of hyperkalemia. Hypokalemia in the surgical patient usually results from unreplaced losses of gastrointestinal fluids (diarrhea, massive emesis) (see Table 4.2 for composition of gastrointestinal fluids). Hypokalemia also may exist or be exaggerated by renal tubular disorders, diuretic use, metabolic alkalosis, some medications, and hormonal disorders (primary aldosteronism, Cushing’s syndrome). The treatment of hypokalemia is directed toward rapid restoration of extracellular potassium concentration followed by slower replenishment of total body deficits. This approach would be appropriate for Case 2. This can be accom- plished by infusion of 20 to 40mEq of potassium/hour and must be accompanied by continuous electrocardiogram (ECG) monitoring at higher rates. Restoration of other abnormalities, such as alkalosis, also should be addressed.

Calcium: Nearly 99% of body calcium is located in bone. Calcium located in body fluid circulates as free (40%) or bound to albumin (50%) or other anions. Only the free component is biologically active. Acid–base abnormalities alter the binding of calcium to albumin. (Alkalosis leads to a reduction in ionized calcium, whereas acidosis increases ionized calcium levels.) Most of the ingested calcium is excreted in stool. Replacement of calcium usually is not necessary for routine, uncomplicated surgical patients. However, attention to replacement may be required in patients with large fluid shifts, immo- bilization, and especially in patients with surgical thyroid or parathy- roid disorders. Hypercalcemia most often results from hyperparathyroidism and malignancy. Symptoms of hypercalcemia may include confusion, lethargy, weakness, anorexia, vomiting, constipation, and pancreatitis. Nephrogenic diabetes insipidus also may result. Serum calcium concentrations above 14mg/dL or any level associated with ECG abnormalities requires urgent treatment. Virtually all such patients, such as the one described in Case 3, are dehydrated and require hydration with saline. Additional treatments may include diuretics as well as diphosphanates, calcitonin, or mithramycin. Steroids may be useful in some patients. Hypocalcemia results from several mechanisms, including low parathormone activity, low vitamin D activity, and conditions referred to as pseudohypocalcemia (low albumin, hyperventilation). Acute conditions such as pancreatitis, massive soft tissue infections, high-output gastrointestinal fistulas, and massive transfusion of citrated blood also may lead to acute hypocalcemia. The early symptoms of hypocalcemia include numbness or tingling of the circumoral region or fingertips. Tetany and seizure may occur at very low calcium levels. Replacement of calcium requires an appreciation of the causes and symptoms. For 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 79

Patient is hyperkalemic

Assess immediate risk. Evaluate renal function. Monitor ECG continuously.

Kidneys are functioning Patient is in renal failure

Initiate dialysis.

Serum potassium < 6.0 mEg/L; no Serum potasslum > 6.0 mEq/L, or ECG changes are present ECG changes are present Administer cation exchange resins. Give Administer cation exchange resins. Give orally if tolerated. If not, give rectally. orally if tolerated. If not, give rectally.

Patient is not receiving Patient is receiving digitalis digitalis

Give 10% calcium gluconate, Give sodium bicarbonate, 10 ml I.V. over 2 min. 45 mEq I.V. over 5 min. If ECG changes persist, repeat over 15 min.

ECG changes resolve ECG changes persist Give sodium bicarbonate, 45mEq I.V. over 5 min. If ECG changes persist, repeat over 15 min.

ECG changes resolve ECG changes persist Give 1 ampule D50W with 10 U regular insulin I.V. over 15 min. If patient is well hydrated, consider furosemide, 20–40 mg I.V.

ECG changes resolve ECG changes persist Initiate dialysis.

Algorithm 4.2. Assessment and treatment of hyperkalemia. (Reprinted from Van Zee KJ, Lowry SF. Life-threatening electrolyte abnormalities. In: Wilmore DW, Cheung LY, Harken AH, et al, eds. ACS Surgery: Principles and Practice (Section 1: Resuscitation). New York: WebMD Corporation, 1997, with permission.) 80 S.F. Lowry

acute symptomatic patients, intravenous replacement may be necessary. Magnesium: Approximately 50% of body magnesium is located in bone and is not readily exchangeable. Like potassium, magnesium is an intracellular cation that tends to become depleted during alkalotic conditions. Magnesium absorption occurs in the small intestine, and the normal dietary intake approximates 20mEq/day. Hypomagnesemia may occur secondary to malabsorption, diarrhea, hypoparathyroidism, pancreatitis, intestinal fistulas, cirrhosis, and hypoaldosteronism. It also may occur during periods of refeeding after catabolism or starvation. Low magnesium levels also often accompany hypocalcemic states, and the symptoms of deficiency are similar. Often, repletion of both ions is necessary to restore normal function. Up to 2mEg/kg daily may be administered in the presence of normal renal function. Attention to restoration of any fluid deficits also is mandatory. Hypermagnesemia most frequently occurs in the presence of renal failure. Acidosis exacerbates this condition. Use of magnesium- containing antacids also may lead to elevated serum levels. Emergency treatment of symptomatic hypermagnesemia requires calcium salts, and definitive treatment may require hydration and renal dialysis. Phosphate: Phosphate is the most abundant intracellular anion, whereas only 0.1% of body phosphate is in the circulation. Conse- quently, blood levels do not reflect total body stores. Hypophosphatemia may result from reduced intestinal absorption, increased renal excretion, hyperparathyroidism, massive liver resec- tion, or inadequate repletion during recovery from starvation or catabolism. Tissue oxygen delivery may be impaired due to reduced 2,3-diphosphoglycerate levels. Muscle weakness and malaise accompany total body depletion. Prolonged supplementation may be necessary in severely depleted patients. Hyperphosphatemia often occurs in the presence of impaired renal function and may be associated with hypocalcemia. Hypoparathy- roidism also reduces renal phosphate excretion.

Summary

Abnormalities of ﬂuid balance, electrolyte imbalance, and acid– base status are very common in surgical patients. While one must address acute, life-threatening abnormalities expeditiously, a systematic approach to evaluating each patient should be a routine component of surgical care. Addressing ﬂuid, electrolyte, and acid–base status is part of the care plan for every patient. The surgeon should antici- pate clinical conditions that can present with or eventuate in such abnormalities. 4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient 81

Selected Readings

Goldborger E. Primer of Water, Electrolyte and Acid–Base Syndromes, 7th ed. Philadelphia: Lea & Febiger, 1986. Nathens AB, Maier RV. In: Norton JA, Bollinger RR, Chang AE. et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001. Pemberton LB, Pemberton PG. Treatment of Water, Electrolyte, and Acid–Base Disorders in the Surgical Patient. New York: McGraw-Hill, 1994. Polk HC, Gardner B, Stone HH. Basic Surgery, 5th ed. St. Louis: Quality Medical Publishing, 1995. Shires GT, Shires GT III, Lowry S. Fluid electrolyte and nutritional management of the surgical patient. In: Schwartz SI, ed. Principles of Surgery, 6th ed. New York: McGraw-Hill, 1994.