Surgery_Schwartz

Surgery_Schwartz. necrosis factor-alpha response. Ann Surg. 2003;237(1):110-115. doi: 10.1097/01.SLA.0000041040.98684.CB 260. van Zanten AR, Hofman Z, Heyland DK. Consequences of the REDOXS and METAPLUS trials: the end of an era of glutamine and antioxidant supplementation for critically ill patients? JPEN J Parenter Enteral Nutr. 2015;39(8):890-892. doi: 10.1177/0148607114567201 261. Luiking YC, Ten Have GA, Wolfe RR, Deutz NE. Arginine de novo and nitric oxide production in disease states. Am J Physiol Endocrinol Metab. 2012;303(10):E1177-E1189. doi: 10.1152/ajpendo.00284.2012 262. Drover JW, Dhaliwal R, Weitzel L, Wischmeyer PE, Ochoa JB, Heyland DK. Perioperative use of arginine-supplemented diets: a systematic review of the evidence. J Am Coll Surg. 2011;212(3):385-399, 99 e1. doi: 10.1016/j.jamcollsurg.2010.10.016 263. Brown B, Roehl K, Betz M. Enteral nutrition for-mula selection: current evidence and implications for practice. Nutr Clin Pract. 2015;30(1):72-85. doi:


Surgery_Schwartz

Surgery_Schwartz. e1. doi: 10.1016/j.jamcollsurg.2010.10.016 263. Brown B, Roehl K, Betz M. Enteral nutrition for-mula selection: current evidence and implications for practice. Nutr Clin Pract. 2015;30(1):72-85. doi: 10.1177/0884533614561791 264. Marik PE, Flemmer M. Immunonutrition in the surgical patient. Minerva Anestesiol. 2012;78(3):336-342. 265. Guidelines CCP. Enteral Feeding Guidelines. 2013. 266. Pontes-Arruda A, Martins LF, de Lima SM, et al. Enteral nutri-tion with eicosapentaenoic acid, gamma-linolenic acid and antioxidants in the early treatment of sepsis: results from a mul-ticenter, prospective, randomized, double-blinded, controlled study: the INTERSEPT study. Crit Care. 2011;15(3):R144. doi: 10.1186/cc10267 267. Choban P, Dickerson R, Malone A, et al. A.S.P.E.N. Clinical guidelines: nutrition support of hospitalized adult patients with obesity. JPEN J Parenter Enteral Nutr. 2013;37(6):714-744. doi: 10.1177/0148607113499374 268. Btaiche IF. Branched-chain amino acids in patients with


Surgery_Schwartz

Surgery_Schwartz. support of hospitalized adult patients with obesity. JPEN J Parenter Enteral Nutr. 2013;37(6):714-744. doi: 10.1177/0148607113499374 268. Btaiche IF. Branched-chain amino acids in patients with hepatic encephalopathy. 1982. Nutr Clin Pract. 2003;18(1):97-100. 269. Patton KM, Aranda-Michel J. Nutritional aspects in liver dis-ease and liver transplantation. Nutr Clin Pract. 2002;17(6): 332-340. 270. Koretz RL, Avenell A, Lipman TO. Nutritional support for liver disease. Cochrane Database Syst Rev. 2012(5):CD008344. doi: 10.1002/14651858.CD008344.pub2 271. DiSario JA, Baskin WN, Brown RD, et al. Endoscopic approaches to enteral nutritional support. Gastrointest Endosc. 2002;55(7):901-908. 272. Heyland DK, Drover JW, Dhaliwal R, Greenwood J. Optimiz-ing the benefits and minimizing the risks of enteral nutrition in the critically ill: role of small bowel feeding. JPEN J Parenter Enteral Nutr. 2002;26(6 suppl):S51-S55; discussion S56S57. 273. Scolapio JS. Methods for decreasing risk of


Surgery_Schwartz

Surgery_Schwartz. of enteral nutrition in the critically ill: role of small bowel feeding. JPEN J Parenter Enteral Nutr. 2002;26(6 suppl):S51-S55; discussion S56S57. 273. Scolapio JS. Methods for decreasing risk of aspiration pneu-monia in critically ill patients. JPEN J Parenter Enteral Nutr. 2002;26(6 suppl):S58-S61; discussion S61. 274. Vanek VW. Ins and outs of enteral access: part 2—long term access—esophagostomy and gastrostomy. Nutr Clin Pract. 2003;18(1):50-74. 275. Mermel LA, Allon M, Bouza E, et al. Clinical practice guide-lines for the diagnosis and management of intravascular catheter-related infection: 2009 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2009;49(1):1-45. doi: 10.1086/599376 276. Quality AfHRa. Tools for reducing central line-associated blood stream infections. Available at: http://www.ahrq.gov/legacy/qual/clabsitools/clabsitools.htm#purpose 277. Maecken T, Grau T. Ultrasound imaging in vascular access. Crit Care Med. 2007;35(5 suppl):S178-S185. doi:


Surgery_Schwartz

Surgery_Schwartz. Available at: http://www.ahrq.gov/legacy/qual/clabsitools/clabsitools.htm#purpose 277. Maecken T, Grau T. Ultrasound imaging in vascular access. Crit Care Med. 2007;35(5 suppl):S178-S185. doi: 10.1097/01.CCM.0000260629.86351.A5Brunicardi_Ch02_p0027-p0082.indd 8201/03/19 6:50 PM


Surgery_Schwartz

Surgery_Schwartz. Introduction 83Body Fluids 83Total Body Water / 83Fluid Compartments / 83Composition of Fluid Compartments / 83Osmotic Pressure / 84Body Fluid Changes 85Normal Exchange of Fluid and Electrolytes / 85Classification of Body Fluid Changes / 85Disturbances in Fluid Balance / 85Volume Control / 86Concentration Changes / 86Composition Changes: Etiology and Diagnosis / 88Acid-Base Balance / 91Metabolic Derangements / 91Fluid and Electrolyte Therapy 93Parenteral Solutions / 93Alternative Resuscitative Fluids / 94Correction of Life-Threatening Electrolyte Abnormalities / 94Preoperative Fluid Therapy / 96Intraoperative Fluid Therapy / 97Postoperative Fluid Therapy / 97Fluid Management in Enhanced Recovery After Surgery (ERAS) Pathways / 97Special Considerations for the Postoperative Patient / 98Electrolyte Abnormalities in Specific Surgical Patients 98Neurologic Patients / 98Malnourished Patients: Refeeding Syndrome / 98Acute Renal Failure Patients / 99Cancer Patients / 99Fluid and


Surgery_Schwartz

Surgery_Schwartz. / 98Electrolyte Abnormalities in Specific Surgical Patients 98Neurologic Patients / 98Malnourished Patients: Refeeding Syndrome / 98Acute Renal Failure Patients / 99Cancer Patients / 99Fluid and Electrolyte Management of the Surgical PatientMatthew D. Neal 3chapterINTRODUCTIONFluid and electrolyte management is paramount to the care of the surgical patient. Changes in both fluid volume and electro-lyte composition occur preoperatively, intraoperatively, and postoperatively, as well as in response to trauma and sepsis. The sections that follow review the normal anatomy of body fluids, electrolyte composition and concentration abnormalities and treatments, common metabolic derangements, and alternative resuscitative fluids. These concepts are then discussed in relationship to management of specific surgical patients and their commonly encountered fluid and electrolyte abnormalities.BODY FLUIDSTotal Body WaterWater constitutes approximately 50% to 60% of total body weight. The


Surgery_Schwartz

Surgery_Schwartz. of specific surgical patients and their commonly encountered fluid and electrolyte abnormalities.BODY FLUIDSTotal Body WaterWater constitutes approximately 50% to 60% of total body weight. The relationship between total body weight and total body water (TBW) is relatively constant for an individual and is primarily a reflection of body fat. Lean tissues such as muscle and solid organs have higher water content than fat and bone. As a result, young, lean males have a higher proportion of body weight as water than elderly or obese individuals. In an average young adult male, TBW accounts for 60% of total body weight, whereas in an average young adult female, it is 50%.1 The lower percent-age of TBW in females correlates with a higher percentage of adipose tissue and lower percentage of muscle mass in most. Estimates of percentage of TBW should be adjusted downward approximately 10% to 20% for obese individuals and upward by 10% for malnourished individuals. The highest percentage of TBW


Surgery_Schwartz

Surgery_Schwartz. mass in most. Estimates of percentage of TBW should be adjusted downward approximately 10% to 20% for obese individuals and upward by 10% for malnourished individuals. The highest percentage of TBW is found in newborns, with approximately 80% of their total body weight comprised of water. This decreases to approximately 65% by 1 year of age and thereafter remains fairly constant.1Fluid CompartmentsTBW is divided into three functional fluid compartments: plasma, extravascular interstitial fluid, and intracellular fluid (Fig. 3-1). The extracellular fluids (ECF), plasma, and intersti-tial fluid together compose about one-third of the TBW, and the intracellular compartment composes the remaining two thirds. The extracellular water composes 20% of the total body weight and is divided between plasma (5% of body weight) and inter-stitial fluid (15% of body weight). Intracellular water makes up approximately 40% of an individual’s total body weight, with the largest proportion in the


Surgery_Schwartz

Surgery_Schwartz. plasma (5% of body weight) and inter-stitial fluid (15% of body weight). Intracellular water makes up approximately 40% of an individual’s total body weight, with the largest proportion in the skeletal muscle mass.Composition of Fluid CompartmentsThe normal chemical composition of the body fluid compart-ments is shown in Fig. 3-2. The ECF compartment is bal-anced between sodium, the principal cation, and chloride and bicarbonate, the principal anions. The intracellular fluid compartment is composed primarily of the cations potassium and magnesium, the anions phosphate and sulfate, and proteins. The concentration gradient between compartments is maintained by adenosine triphosphate–driven sodium-potassium pumps located within the cell membranes. The composition of the plasma and interstitial fluid differs only slightly in ionic compo-sition. The slightly higher protein content (organic anions) in plasma results in a higher plasma cation composition relative to the interstitial fluid,


Surgery_Schwartz

Surgery_Schwartz. fluid differs only slightly in ionic compo-sition. The slightly higher protein content (organic anions) in plasma results in a higher plasma cation composition relative to the interstitial fluid, as explained by the Gibbs-Donnan equilib-rium equation. Proteins add to the osmolality of the plasma and contribute to the balance of forces that determine fluid balance across the capillary endothelium. Although the movement of ions and proteins between the various fluid compartments is restricted, water is freely diffusible. Water is distributed evenly throughout all fluid compartments of the body so that a given volume of water increases the volume of any one compartment 2Brunicardi_Ch03_p0083-p0102.indd 8308/12/18 10:07 AM 84Figure 3-1. Functional body fluid compartments. TBW = total body water.Key Points1 Proper management of fluid and electrolytes facilitates cru-cial homeostasis that allows cardiovascular perfusion, organ system function, and cellular mechanisms to respond to


Surgery_Schwartz

Surgery_Schwartz. body water.Key Points1 Proper management of fluid and electrolytes facilitates cru-cial homeostasis that allows cardiovascular perfusion, organ system function, and cellular mechanisms to respond to sur-gical illness.2 Knowledge of the compartmentalization of body fluids forms the basis for understanding pathologic shifts in these fluid spaces in disease states. Although difficult to quantify, a deficiency in the functional extracellular fluid compart-ment often requires resuscitation with isotonic fluids in sur-gical and trauma patients.3 Alterations in the concentration of serum sodium have pro-found effects on cellular function due to water shifts between the intracellular and extracellular spaces.4 Different rates of compensation between respiratory and metabolic components of acid-base homeostasis require fre-quent laboratory reassessment during therapy.5 Although active investigation continues, alternative resusci-tation fluids have limited clinical utility, other than the


Surgery_Schwartz

Surgery_Schwartz. homeostasis require fre-quent laboratory reassessment during therapy.5 Although active investigation continues, alternative resusci-tation fluids have limited clinical utility, other than the cor-rection of specific electrolyte abnormalities.6 Enhanced recovery after surgery (ERAS) protocols have markedly changed perioperative fluid management and are being used more frequently. ERAS minimizes perioperative fluid administration and focuses on early enteral intake to reduce morbidity associated with IV fluid administration.7 Most acute surgical illnesses are accompanied by some degree of volume loss or redistribution. Consequently, iso-tonic fluid administration is the most common initial intra-venous fluid strategy, while attention is being given to alterations in concentration and composition.8 Some surgical patients with neurologic illness, malnutrition, acute renal failure, or cancer require special attention to well-defined, disease-specific abnormalities in fluid and electrolyte


Surgery_Schwartz

Surgery_Schwartz. surgical patients with neurologic illness, malnutrition, acute renal failure, or cancer require special attention to well-defined, disease-specific abnormalities in fluid and electrolyte status.% of Total body weightPlasma 5%Interstitialfluid 15%Intracellularvolume 40%Volume of TBWExtracellular volumePlasmaInterstitialIntracellular volume14,000 mL3500 mL10,500 mL28,000 mL42,000 mLMale (70 kg)10,000 mL2500 mL7500 mL20,000 mL30,000 mLFemale (60 kg)relatively little. Sodium, however, is confined to the ECF com-partment, and because of its osmotic and electrical properties, it remains associated with water. Therefore, sodium-containing fluids are distributed throughout the ECF and add to the volume of both the intravascular and interstitial spaces. Although the administration of sodium-containing fluids expands the intra-vascular volume, it also expands the interstitial space by approx-imately three times as much as the plasma.Osmotic PressureThe physiologic activity of electrolytes in


Surgery_Schwartz

Surgery_Schwartz. fluids expands the intra-vascular volume, it also expands the interstitial space by approx-imately three times as much as the plasma.Osmotic PressureThe physiologic activity of electrolytes in solution depends on the number of particles per unit volume (millimoles per liter, or mmol/L), the number of electric charges per unit volume (milli-equivalents per liter, or mEq/L), and the number of osmotically active ions per unit volume (milliosmoles per liter, or mOsm/L). The concentration of electrolytes usually is expressed in terms of the chemical combining activity, or equivalents. An equiva-lent of an ion is its atomic weight expressed in grams divided by the valence:Equivalent = atomic weight (g)/valenceFor univalent ions such as sodium, 1 mEq is same as 1 mmol. For divalent ions such as magnesium, 1 mmol equals 2 mEq. The number of milliequivalents of cations must be bal-anced by the same number of milliequivalents of anions. How-ever, the expression of molar equivalents alone does


Surgery_Schwartz

Surgery_Schwartz. magnesium, 1 mmol equals 2 mEq. The number of milliequivalents of cations must be bal-anced by the same number of milliequivalents of anions. How-ever, the expression of molar equivalents alone does not allow a physiologic comparison of solutes in a solution.The movement of water across a cell membrane depends primarily on osmosis. To achieve osmotic equilibrium, water moves across a semipermeable membrane to equalize the con-centration on both sides. This movement is determined by the concentration of the solutes on each side of the membrane. Osmotic pressure is measured in units of osmoles (osm) or milliosmoles (mOsm) that refer to the actual number of osmotically active particles. For example, 1 mmol of sodium chloride contributes to 2 mOsm (one from sodium and one from chloride). The principal determinants of osmolality are the concentrations of sodium, glucose, and urea (blood urea nitrogen, or BUN):Calculated serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8)The osmolality


Surgery_Schwartz

Surgery_Schwartz. principal determinants of osmolality are the concentrations of sodium, glucose, and urea (blood urea nitrogen, or BUN):Calculated serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8)The osmolality of the intracellular and extracellular fluids is maintained between 290 and 310 mOsm in each compart-ment. Because cell membranes are permeable to water, any Brunicardi_Ch03_p0083-p0102.indd 8408/12/18 10:07 AM 85FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTCHAPTER 3change in osmotic pressure in one compartment is accompanied by a redistribution of water until the effective osmotic pressure between compartments is equal. For practical clinical purposes, most significant gains and losses of body fluid are directly from the extracellular compartment.BODY FLUID CHANGESNormal Exchange of Fluid and ElectrolytesThe healthy person consumes an average of 2000 mL of water per day, approximately 75% from oral intake and the rest extracted from solid foods. Daily water losses include


Surgery_Schwartz

Surgery_Schwartz. of Fluid and ElectrolytesThe healthy person consumes an average of 2000 mL of water per day, approximately 75% from oral intake and the rest extracted from solid foods. Daily water losses include 800 to 1200 mL in urine, 250 mL in stool, and 600 mL in insensible losses. Insensible losses of water occur through both the skin (75%) and lungs (25%) and can be increased by such factors as fever, hypermetabolism, and hyperventilation. Sensible water losses such as sweating or pathologic loss of gastrointestinal (GI) fluids vary widely, but these include the loss of electrolytes as well as water (Table 3-1). To clear the products of metabo-lism, the kidneys must excrete a minimum of 500 to 800 mL of urine per day, regardless of the amount of oral intake.The typical individual consumes 3 to 5 g of dietary salt per day, with the balance maintained by the kidneys. With hypo-natremia or hypovolemia, sodium excretion can be reduced to as little as 1 mEq/d or maximized to as much as 5000 mEq/d to


Surgery_Schwartz

Surgery_Schwartz. dietary salt per day, with the balance maintained by the kidneys. With hypo-natremia or hypovolemia, sodium excretion can be reduced to as little as 1 mEq/d or maximized to as much as 5000 mEq/d to achieve balance except in people with salt-wasting kidneys. Sweat is hypotonic, and sweating usually results in only a small sodium loss. GI losses are isotonic to slightly hypotonic and contribute little to net gain or loss of free water when measured and appropriately replaced by isotonic salt solutions.Classification of Body Fluid ChangesDisorders in fluid balance may be classified into three general categories: disturbances in (a) volume, (b) concentration, and (c) composition. Although each of these may occur simultaneously, each is a separate entity with unique mechanisms demanding individual correction. Isotonic gain or loss of salt solution results in extracellular volume changes, with little impact on intracellular fluid volume. If free water is added or lost from the ECF, water


Surgery_Schwartz

Surgery_Schwartz. correction. Isotonic gain or loss of salt solution results in extracellular volume changes, with little impact on intracellular fluid volume. If free water is added or lost from the ECF, water will pass between the ECF and intracellular fluid until solute concentration or osmolarity is equalized between the compartments. Unlike with sodium, the concentration of most other ions in the ECF can be altered without significant change in the total number of osmotically active particles, producing only a compositional change.Disturbances in Fluid BalanceExtracellular volume deficit is the most common fluid disorder in surgical patients and can be either acute or chronic. Acute volume deficit is associated with cardiovascular and central ner-vous system signs, whereas chronic deficits display tissue signs, such as a decrease in skin turgor and sunken eyes, in addition to cardiovascular and central nervous system signs (Table 3-2). Laboratory examination may reveal an elevated BUN level if the


Surgery_Schwartz

Surgery_Schwartz. signs, such as a decrease in skin turgor and sunken eyes, in addition to cardiovascular and central nervous system signs (Table 3-2). Laboratory examination may reveal an elevated BUN level if the deficit is severe enough to reduce glomerular filtration and hemoconcentration. Urine osmolality usually will be higher than serum osmolality, and urine sodium will be low, typically <20 mEq/L. Serum sodium concentration does not necessar-ily reflect volume status and therefore may be high, normal, or low when a volume deficit is present. The most common cause of volume deficit in surgical patients is a loss of GI flu-ids (Table 3-3) from nasogastric suction, vomiting, diarrhea, or Figure 3-2. Chemical composition of body fluid compartments.PlasmaCATIONS154 mEq/L154 mEq/LCI−SO42–PO43–ProteinOrganicacids103HCO3−273516Na+142K+4Ca2+5Mg2+3ANIONSInterstitialfluidCATIONS153 mEq/L153 mEq/LCI−PO43–SO42–ProteinOrganicacids114HCO3−30531Na+144K+4Ca2+3Mg2+2ANIONSIntracellularfluidCATIONS200 mEq/L200


Surgery_Schwartz

Surgery_Schwartz. mEq/L153 mEq/LCI−PO43–SO42–ProteinOrganicacids114HCO3−30531Na+144K+4Ca2+3Mg2+2ANIONSIntracellularfluidCATIONS200 mEq/L200 mEq/LK+150ProteinHCO3−SO42–HPO43–1015040Mg2+40Na+10ANIONSBrunicardi_Ch03_p0083-p0102.indd 8508/12/18 10:07 AM 86BASIC CONSIDERATIONSPART Ienterocutaneous fistula. In addition, sequestration secondary to soft tissue injuries, burns, and intra-abdominal processes such as peritonitis, obstruction, or prolonged surgery can also lead to massive volume deficits.Extracellular volume excess may be iatrogenic or second-ary to renal dysfunction, congestive heart failure, or cirrhosis. Both plasma and interstitial volumes usually are increased. Symptoms are primarily pulmonary and cardiovascular (see Table 3-2). In fit patients, edema and hyperdynamic circula-tion are common and well tolerated. However, the elderly and patients with cardiac disease may quickly develop congestive heart failure and pulmonary edema in response to only a moder-ate volume excess.Volume


Surgery_Schwartz

Surgery_Schwartz. common and well tolerated. However, the elderly and patients with cardiac disease may quickly develop congestive heart failure and pulmonary edema in response to only a moder-ate volume excess.Volume ControlVolume changes are sensed by both osmoreceptors and baro-receptors. Osmoreceptors are specialized sensors that detect even small changes in fluid osmolality and drive changes in thirst and diuresis through the kidneys.2 For example, when plasma osmolality is increased, thirst is stimulated and water consumption increases, although the exact cell mechanism is not known.3 Additionally, the hypothalamus is stimulated to secrete vasopressin, which increases water reabsorption in the kidneys. Together, these two mechanisms return the plasma osmolality to normal. Baroreceptors also modulate volume in response to changes in pressure and circulating volume through specialized pressure sensors located in the aortic arch and carotid sinuses.4 Baroreceptor responses are both neural, through


Surgery_Schwartz

Surgery_Schwartz. volume in response to changes in pressure and circulating volume through specialized pressure sensors located in the aortic arch and carotid sinuses.4 Baroreceptor responses are both neural, through sympathetic and parasympathetic pathways, and hormonal, through substances including renin-angiotensin, aldosterone, atrial natriuretic pep-tide, and renal prostaglandins. The net result of alterations in renal sodium excretion and free water reabsorption is restoration of volume to the normal state.Concentration ChangesChanges in serum sodium concentration are inversely propor-tional to TBW. Therefore, abnormalities in TBW are reflected by abnormalities in serum sodium levels.Hyponatremia. A low serum sodium level occurs when there is an excess of extracellular water relative to sodium. Extracel-lular volume can be high, normal, or low (Fig. 3-3). In most cases of hyponatremia, sodium concentration is decreased as a consequence of either sodium depletion or dilution.5 Dilutional


Surgery_Schwartz

Surgery_Schwartz. Extracel-lular volume can be high, normal, or low (Fig. 3-3). In most cases of hyponatremia, sodium concentration is decreased as a consequence of either sodium depletion or dilution.5 Dilutional hyponatremia frequently results from excess extracellular water and therefore is associated with a high extracellular volume status. Excessive oral water intake or iatrogenic intravenous (IV) excess free water administration can cause hyponatremia. Post-operative patients are particularly prone to increased secretion of antidiuretic hormone (ADH), which increases reabsorption 3Table 3-2Signs and symptoms of volume disturbancesSYSTEMVOLUME DEFICITVOLUME EXCESSGeneralizedWeight lossWeight gain Decreased skin turgorPeripheral edemaCardiacTachycardiaIncreased cardiac output Orthostasis/hypotensionIncreased central venous pressure Collapsed neck veinsDistended neck veins MurmurRenalOliguria— Azotemia GIIleusBowel edemaPulmonary—Pulmonary edemaTable 3-1Water exchange (60to 80-kg man)ROUTESAVERAGE


Surgery_Schwartz

Surgery_Schwartz. central venous pressure Collapsed neck veinsDistended neck veins MurmurRenalOliguria— Azotemia GIIleusBowel edemaPulmonary—Pulmonary edemaTable 3-1Water exchange (60to 80-kg man)ROUTESAVERAGE DAILY VOLUME (mL)MINIMAL (mL)MAXIMAL (mL)H2O gain: Sensible: Oral fluids800–150001500/h Solid foods500–70001500 Insensible: Water of oxidation250125800 Water of solution00500H2O loss: Sensible: Urine800–15003001400/h Intestinal0–25002500/h Sweat004000/h Insensible: Lungs and skin6006001500Brunicardi_Ch03_p0083-p0102.indd 8608/12/18 10:07 AM 87FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTCHAPTER 3of free water from the kidneys with subsequent volume expan-sion and hyponatremia. This is usually self-limiting in that both hyponatremia and volume expansion decrease ADH secretion. Additionally, a number of drugs can cause water retention and subsequent hyponatremia, such as antipsychotics and tricyclic antidepressants as well as angiotensin-converting enzyme


Surgery_Schwartz

Surgery_Schwartz. ADH secretion. Additionally, a number of drugs can cause water retention and subsequent hyponatremia, such as antipsychotics and tricyclic antidepressants as well as angiotensin-converting enzyme inhib-itors. The elderly are particularly susceptible to drug-induced hyponatremia. Physical signs of volume overload usually are absent, and laboratory evaluation reveals hemodilution. Deple-tional causes of hyponatremia are associated with either a decreased intake or increased loss of sodium-containing fluids. A concomitant ECF volume deficit is common. Causes include decreased sodium intake, such as consumption of a low-sodium diet or use of enteral feeds, which are typically low in sodium; Table 3-3Composition of GI secretionsTYPE OF SECRETIONVOLUME (mL/24 h)NA (mEq/L)K (mEq/L)CL (mEq/L)HCO3− (mEq/L)Stomach1000–200060–9010–30100–1300Small intestine2000–3000120–1405–1090–12030–40Colon—6030400Pancreas600–800135–1455–1070–9095–115Bile300–800135–1455–1090–11030–40Figure 3-3. Evaluation of


Surgery_Schwartz

Surgery_Schwartz. (mEq/L)Stomach1000–200060–9010–30100–1300Small intestine2000–3000120–1405–1090–12030–40Colon—6030400Pancreas600–800135–1455–1070–9095–115Bile300–800135–1455–1090–11030–40Figure 3-3. Evaluation of sodium abnormalities. ADH = antidiuretic hormone; SIADH = syndrome of inappropriate secretion of antidi-uretic hormone.HighIncreased intakePostoperative ADH secretionDrugsHighIatrogenic sodium administrationMineralocorticoid excessAldosteronismCushing’s diseaseCongenital adrenal hyperplasiaHyponatremiaVolume statusNormalHyperglycemia˜Plasma lipids/proteinsSIADHWater intoxicationDiureticsHypernatremiaVolume statusNormalNonrenal water lossSkinGIRenal water lossRenal diseaseDiureticsDiabetes insipidusLowDecreased sodium intakeGI lossesRenal lossesDiureticsPrimary renal diseaseLowNonrenal water lossSkinGI Renal water lossRenal (tubular) diseaseOsmotic diureticsDiabetes insipidusAdrenal failureBrunicardi_Ch03_p0083-p0102.indd 8708/12/18 10:07 AM 88BASIC CONSIDERATIONSPART IGI losses from


Surgery_Schwartz

Surgery_Schwartz. lossSkinGI Renal water lossRenal (tubular) diseaseOsmotic diureticsDiabetes insipidusAdrenal failureBrunicardi_Ch03_p0083-p0102.indd 8708/12/18 10:07 AM 88BASIC CONSIDERATIONSPART IGI losses from vomiting, prolonged nasogastric suctioning, or diarrhea; and renal losses due to diuretic use or primary renal disease.Hyponatremia also can be seen with an excess of solute relative to free water, such as with untreated hyperglycemia or mannitol administration. When hyponatremia in the presence of hyperglycemia is being evaluated, the corrected sodium concen-tration should be calculated as follows:For every 100-mg/dL increment in plasma glucose above normal, the plasma sodium should decrease by 1.6 mEq/LLastly, extreme elevations in plasma lipids and proteins can cause pseudohyponatremia because there is no true decrease in extracellular sodium relative to water.Signs and symptoms of hyponatremia (Table 3-4) are dependent on the degree of hyponatremia and the rapidity with which it


Surgery_Schwartz

Surgery_Schwartz. because there is no true decrease in extracellular sodium relative to water.Signs and symptoms of hyponatremia (Table 3-4) are dependent on the degree of hyponatremia and the rapidity with which it occurred. Clinical manifestations primarily have a central nervous system origin and are related to cellular water intoxication and associated increases in intracranial pressure. Oliguric renal failure also can be a rapid complication in the setting of severe hyponatremia.A systematic review of the etiology of hyponatremia should reveal its cause in a given instance. Hyperosmolar causes, including hyperglycemia or mannitol infusion and pseu-dohyponatremia, should be easily excluded. Next, depletional versus dilutional causes of hyponatremia are evaluated. In the absence of renal disease, depletion is associated with low urine sodium levels (<20 mEq/L), whereas renal sodium wasting shows high urine sodium levels (>20 mEq/L). Dilutional causes of hyponatremia usually are associated with


Surgery_Schwartz

Surgery_Schwartz. is associated with low urine sodium levels (<20 mEq/L), whereas renal sodium wasting shows high urine sodium levels (>20 mEq/L). Dilutional causes of hyponatremia usually are associated with hypervolemic cir-culation. A normal volume status in the setting of hyponatremia should prompt an evaluation for a syndrome of inappropriate secretion of ADH.Hypernatremia. Hypernatremia results from either a loss of free water or a gain of sodium in excess of water. Like hypo-natremia, it can be associated with an increased, normal, or decreased extracellular volume (see Fig. 3-3). Hypervolemic hypernatremia usually is caused either by iatrogenic adminis-tration of sodium-containing fluids, including excess sodium bicarbonate, or mineralocorticoid as seen in hyperaldosteronism, Cushing’s syndrome, and congenital adrenal hyperplasia. Urine sodium concentration is typically >20 mEq/L, and urine osmo-larity is >300 mOsm/L. Normovolemic hypernatremia can result from renal causes, including diabetes


Surgery_Schwartz

Surgery_Schwartz. congenital adrenal hyperplasia. Urine sodium concentration is typically >20 mEq/L, and urine osmo-larity is >300 mOsm/L. Normovolemic hypernatremia can result from renal causes, including diabetes insipidus, diuretic use, and renal disease, or from nonrenal water loss from the GI tract or skin, although the same conditions can result in hypovolemic hypernatremia. When hypovolemia is present, the urine sodium concentration is <20 mEq/L and urine osmolarity is <300 to 400 mOsm/L. Nonrenal water loss can occur secondary to rela-tively isotonic GI fluid losses such as that caused by diarrhea, to hypotonic skin fluid losses such as loss due to fever, or to losses via tracheotomies during hyperventilation. Additionally, thyrotoxicosis can cause water loss, as can the use of hyper-tonic glucose solutions for peritoneal dialysis. With nonrenal water loss, the urine sodium concentration is <15 mEq/L, and the urine osmolarity is >400 mOsm/L.Symptomatic hypernatremia usually occurs only in


Surgery_Schwartz

Surgery_Schwartz. solutions for peritoneal dialysis. With nonrenal water loss, the urine sodium concentration is <15 mEq/L, and the urine osmolarity is >400 mOsm/L.Symptomatic hypernatremia usually occurs only in patients with impaired thirst or restricted access to fluid because thirst will result in increased water intake. Symptoms are rare until the serum sodium concentration exceeds 160 mEq/L but, once present, are associated with significant morbidity and mortality. Because symptoms are related to hyperosmolarity, central nervous system effects predominate (see Table 3-4). Water shifts from the intracellular to the extracellular space in response to a hyperosmolar extracellular space, which results in cellular dehydration. This can put traction on the cerebral vessels and lead to subarachnoid hemorrhage. Central nervous system symptoms can range from restlessness and irritability to seizures, coma, and death. The classic signs of hypovolemic hypernatremia (tachycardia, orthostasis, and


Surgery_Schwartz

Surgery_Schwartz. hemorrhage. Central nervous system symptoms can range from restlessness and irritability to seizures, coma, and death. The classic signs of hypovolemic hypernatremia (tachycardia, orthostasis, and hypotension) may be present, as well as the unique findings of dry, sticky mucous membranes.Composition Changes: Etiology and DiagnosisPotassium Abnormalities. The average dietary intake of potassium is approximately 50 to 100 mEq/d, which in the absence of hypokalemia is excreted primarily in the urine. Extra-cellular potassium is maintained within a narrow range, princi-pally by renal excretion of potassium, which can range from 10 to 700 mEq/d. Although only 2% of the total body potassium (4.5 mEq/L × 14 L = 63 mEq) is located within the extracellular compartment, this small amount is critical to cardiac and neu-romuscular function; thus, even minor changes can have major effects on cardiac activity. The intracellular and extracellular distribution of potassium is influenced by a number


Surgery_Schwartz

Surgery_Schwartz. to cardiac and neu-romuscular function; thus, even minor changes can have major effects on cardiac activity. The intracellular and extracellular distribution of potassium is influenced by a number of factors, including surgical stress, injury, acidosis, and tissue catabolism.Table 3-4Clinical manifestations of abnormalities in serum sodium levelBODY SYSTEMHYPONATREMIACentral nervous systemHeadache, confusion, hyperactive or hypoactive deep tendon reflexes, seizures, coma, increased intracranial pressureMusculoskeletalWeakness, fatigue, muscle cramps/twitchingGIAnorexia, nausea, vomiting, watery diarrheaCardiovascularHypertension and bradycardia if intracranial pressure increases significantlyTissueLacrimation, salivationRenalOliguriaBODY SYSTEMHYPERNATREMIACentral nervous systemRestlessness, lethargy, ataxia, irritability, tonic spasms, delirium, seizures, comaMusculoskeletalWeaknessCardiovascularTachycardia, hypotension, syncopeTissueDry sticky mucous membranes, red swollen tongue,


Surgery_Schwartz

Surgery_Schwartz. lethargy, ataxia, irritability, tonic spasms, delirium, seizures, comaMusculoskeletalWeaknessCardiovascularTachycardia, hypotension, syncopeTissueDry sticky mucous membranes, red swollen tongue, decreased saliva and tearsRenalOliguriaMetabolicFeverBrunicardi_Ch03_p0083-p0102.indd 8808/12/18 10:07 AM 89FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTCHAPTER 3Hyperkalemia Hyperkalemia is defined as a serum potassium concentration above the normal range of 3.5 to 5.0 mEq/L. It is caused by excessive potassium intake, increased release of potassium from cells, or impaired potassium excretion by the kidneys (Table 3-5).6 Increased intake can be either from oral or IV supplementation, or from red cell lysis after transfu-sion. Hemolysis, rhabdomyolysis, and crush injuries can dis-rupt cell membranes and release intracellular potassium into the ECF. Acidosis and a rapid rise in extracellular osmolality from hyperglycemia or IV mannitol can raise serum potassium levels by causing


Surgery_Schwartz

Surgery_Schwartz. cell membranes and release intracellular potassium into the ECF. Acidosis and a rapid rise in extracellular osmolality from hyperglycemia or IV mannitol can raise serum potassium levels by causing a shift of potassium ions to the extracellular compartment.7 Because 98% of total body potassium is in the intracellular fluid compartment, even small shifts of intracel-lular potassium out of the intracellular fluid compartment can lead to a significant rise in extracellular potassium. A number of medications can contribute to hyperkalemia, particularly in the presence of renal insufficiency, including potassium-sparing diuretics, angiotensin-converting enzyme inhibitors, and non-steroidal anti-inflammatory drugs (NSAIDs). Spironolactone and angiotensin-converting enzyme inhibitors interfere with aldosterone activity, inhibiting the normal renal mechanism of potassium excretion. Acute and chronic renal insufficiency also impairs potassium excretion.Symptoms of hyperkalemia are primarily GI,


Surgery_Schwartz

Surgery_Schwartz. aldosterone activity, inhibiting the normal renal mechanism of potassium excretion. Acute and chronic renal insufficiency also impairs potassium excretion.Symptoms of hyperkalemia are primarily GI, neuromus-cular, and cardiovascular (Table 3-6). GI symptoms include nausea, vomiting, intestinal colic, and diarrhea. Neuromuscu-lar symptoms range from weakness to ascending paralysis to respiratory failure. Early cardiovascular signs may be appar-ent from electrocardiogram (ECG) changes and eventually lead to hemodynamic symptoms of arrhythmia and cardiac arrest. ECG changes that may be seen with hyperkalemia include high peaked T waves (early), widened QRS complex, flattened P wave, prolonged PR interval (first-degree block), sine wave formation, and ventricular fibrillation.Hypokalemia Hypokalemia is much more common than hyper-kalemia in the surgical patient. It may be caused by inadequate potassium intake; excessive renal potassium excretion; potas-sium loss in pathologic GI


Surgery_Schwartz

Surgery_Schwartz. is much more common than hyper-kalemia in the surgical patient. It may be caused by inadequate potassium intake; excessive renal potassium excretion; potas-sium loss in pathologic GI secretions, such as with diarrhea, fis-tulas, vomiting, or high nasogastric output; or intracellular shifts from metabolic alkalosis or insulin therapy (see Table 3-5). Table 3-5 Etiology of potassium abnormalitiesHyperkalemiaIncreased intake Potassium supplementation Blood transfusions Endogenous load/destruction: hemolysis, rhabdomyolysis, crush injury, gastrointestinal hemorrhageIncreased release Acidosis Rapid rise of extracellular osmolality (hyperglycemia or mannitol)Impaired excretion Potassium-sparing diuretics Renal insufficiency/failureHypokalemiaInadequate intake Dietary, potassium-free intravenous fluids, potassium deficient TPNExcessive potassium excretion Hyperaldosteronism MedicationsGI losses Direct loss of potassium from GI fluid (diarrhea) Renal loss of potassium (to conserve sodium


Surgery_Schwartz

Surgery_Schwartz. fluids, potassium deficient TPNExcessive potassium excretion Hyperaldosteronism MedicationsGI losses Direct loss of potassium from GI fluid (diarrhea) Renal loss of potassium (to conserve sodium in response to gastric losses)Table 3-6Clinical manifestations of abnormalities in potassium, magnesium, and calcium levelsINCREASED SERUM LEVELSSYSTEMPOTASSIUMMAGNESIUMCALCIUMGINausea/vomiting, colic, diarrheaNausea/vomitingAnorexia, nausea/vomiting, abdominal painNeuromuscularWeakness, paralysis, respiratory failureWeakness, lethargy, decreased reflexesWeakness, confusion, coma, bone painCardiovascularArrhythmia, arrestHypotension, arrestHypertension, arrhythmia, polyuriaRenal——PolydipsiaDECREASED SERUM LEVELSSYSTEMPOTASSIUMMAGNESIUMCALCIUMGIIleus, constipation——NeuromuscularDecreased reflexes, fatigue, weakness, paralysisHyperactive reflexes, muscle tremors, tetany, seizuresHyperactive reflexes, paresthesias, carpopedal spasm, seizuresCardiovascularArrestArrhythmiaHeart


Surgery_Schwartz

Surgery_Schwartz. reflexes, fatigue, weakness, paralysisHyperactive reflexes, muscle tremors, tetany, seizuresHyperactive reflexes, paresthesias, carpopedal spasm, seizuresCardiovascularArrestArrhythmiaHeart failureBrunicardi_Ch03_p0083-p0102.indd 8908/12/18 10:07 AM 90BASIC CONSIDERATIONSPART IThe change in potassium associated with alkalosis can be calcu-lated by the following formula:Potassium decreases by 0.3 mEq/L for every 0.1 increase in pH above normal.Additionally, drugs such as amphotericin, aminoglyco-sides, cisplatin, and ifosfamide that induce magnesium depletion cause renal potassium wastage.8,9 In cases in which potassium deficiency is due to magnesium depletion,10 potassium repletion is difficult unless hypomagnesemia is first corrected.The symptoms of hypokalemia (see Table 3-6), like those of hyperkalemia, are primarily related to failure of normal con-tractility of GI smooth muscle, skeletal muscle, and cardiac mus-cle. Findings may include ileus, constipation, weakness,


Surgery_Schwartz

Surgery_Schwartz. like those of hyperkalemia, are primarily related to failure of normal con-tractility of GI smooth muscle, skeletal muscle, and cardiac mus-cle. Findings may include ileus, constipation, weakness, fatigue, diminished tendon reflexes, paralysis, and cardiac arrest. In the setting of ECF depletion, symptoms may be masked initially and then worsened by further dilution during volume repletion. ECG changes suggestive of hypokalemia include U waves, T-wave flattening, ST-segment changes, and arrhythmias (with digitalis therapy).Calcium Abnormalities. The vast majority of the body’s calcium is contained within the bone matrix, with <1% found in the ECF. Serum calcium is distributed among three forms: protein found (40%), complexed to phosphate and other anions (10%), and ionized (50%). It is the ionized fraction that is responsible for neuromuscular stability and can be measured directly. When total serum calcium levels are measured, the albumin concentration must be taken into


Surgery_Schwartz

Surgery_Schwartz. It is the ionized fraction that is responsible for neuromuscular stability and can be measured directly. When total serum calcium levels are measured, the albumin concentration must be taken into consideration:Adjust total serum calcium down by 0.8 mg/dL for every 1 g/dL decrease in albumin.Unlike changes in albumin, changes in pH will affect the ionized calcium concentration. Acidosis decreases protein bind-ing, thereby increasing the ionized fraction of calcium.Daily calcium intake is 1 to 3 g/d. Most of this is excreted via the bowel, with urinary excretion relatively low. Total body calcium balance is under complex hormonal control, but distur-bances in metabolism are relatively long term and less important in the acute surgical setting. However, attention to the critical role of ionized calcium in neuromuscular function often is required.Hypercalcemia Hypercalcemia is defined as a serum calcium level above the normal range of 8.5 to 10.5 mEq/L or an increase in the ionized


Surgery_Schwartz

Surgery_Schwartz. ionized calcium in neuromuscular function often is required.Hypercalcemia Hypercalcemia is defined as a serum calcium level above the normal range of 8.5 to 10.5 mEq/L or an increase in the ionized calcium level above 4.2 to 4.8 mg/dL. Primary hyperparathyroidism in the outpatient setting and malignancy in hospitalized patients, from either bony metastasis or secre-tion of parathyroid hormone–related protein, account for most cases of symptomatic hypercalcemia.11 Symptoms of hypercal-cemia (see Table 3-6), which vary with the degree of sever-ity, include neurologic impairment, musculoskeletal weakness and pain, renal dysfunction, GI symptoms of nausea, vomiting, and abdominal pain. Cardiac symptoms can be manifested as hypertension, cardiac arrhythmias, and a worsening of digitalis toxicity. ECG changes in hypercalcemia include shortened QT interval, prolonged PR and QRS intervals, increased QRS volt-age, T-wave flattening and widening, and atrioventricular block (which can progress


Surgery_Schwartz

Surgery_Schwartz. ECG changes in hypercalcemia include shortened QT interval, prolonged PR and QRS intervals, increased QRS volt-age, T-wave flattening and widening, and atrioventricular block (which can progress to complete heart block and cardiac arrest).Hypocalcemia Hypocalcemia is defined as a serum calcium level below 8.5 mEq/L or a decrease in the ionized calcium level below 4.2 mg/dL. The causes of hypocalcemia include pancreatitis, massive soft tissue infections such as necrotizing fasciitis, renal failure, pancreatic and small bowel fistulas, hypo-parathyroidism, toxic shock syndrome, abnormalities in mag-nesium levels, and tumor lysis syndrome. In addition, transient hypocalcemia commonly occurs after removal of a parathyroid adenoma due to atrophy of the remaining glands and avid bone remineralization, and sometimes requires high-dose calcium supplementation.12 Additionally, malignancies associated with increased osteoblastic activity, such as breast and prostate can-cer, can lead to


Surgery_Schwartz

Surgery_Schwartz. and sometimes requires high-dose calcium supplementation.12 Additionally, malignancies associated with increased osteoblastic activity, such as breast and prostate can-cer, can lead to hypocalcemia from increased bone formation.13 Calcium precipitation with organic anions is also a cause of hypocalcemia and may occur during hyperphosphatemia from tumor lysis syndrome or rhabdomyolysis. Pancreatitis may sequester calcium via chelation with free fatty acids. Massive blood transfusion with citrate binding is another mechanism.14,15 Hypocalcemia rarely results solely from decreased intake because bone reabsorption can maintain normal levels for pro-longed periods.Asymptomatic hypocalcemia may occur when hypopro-teinemia results in a normal ionized calcium level. Conversely, symptoms can develop with a normal serum calcium level during alkalosis, which decreases ionized calcium. In general, neuromuscular and cardiac symptoms do not occur until the ion-ized fraction falls below 2.5 mg/dL


Surgery_Schwartz

Surgery_Schwartz. with a normal serum calcium level during alkalosis, which decreases ionized calcium. In general, neuromuscular and cardiac symptoms do not occur until the ion-ized fraction falls below 2.5 mg/dL (see Table 3-6). Clinical findings may include paresthesias of the face and extremities, muscle cramps, carpopedal spasm, stridor, tetany, and seizures. Patients will demonstrate hyperreflexia and may exhibit positive Chvostek’s sign (spasm resulting from tapping over the facial nerve) and Trousseau’s sign (spasm resulting from pressure applied to the nerves and vessels of the upper extremity with a blood pressure cuff). Hypocalcemia may lead to decreased cardiac contractility and heart failure. ECG changes of hypocal-cemia include prolonged QT interval, T-wave inversion, heart block, and ventricular fibrillation.Phosphorus Abnormalities. Phosphorus is the primary intra-cellular divalent anion and is abundant in metabolically active cells. Phosphorus is involved in energy production during


Surgery_Schwartz

Surgery_Schwartz. fibrillation.Phosphorus Abnormalities. Phosphorus is the primary intra-cellular divalent anion and is abundant in metabolically active cells. Phosphorus is involved in energy production during gly-colysis and is found in high-energy phosphate products such as adenosine triphosphate. Serum phosphate levels are tightly controlled by renal excretion.Hyperphosphatemia Hyperphosphatemia can be due to decreased urinary excretion, increased intake, or endogenous mobilization of phosphorus. Most cases of hyperphosphatemia are seen in patients with impaired renal function. Hypoparathy-roidism or hyperthyroidism also can decrease urinary excretion of phosphorus and thus lead to hyperphosphatemia. Increased release of endogenous phosphorus can be seen in association with any clinical condition that results in cell destruction, includ-ing rhabdomyolysis, tumor lysis syndrome, hemolysis, sepsis, severe hypothermia, and malignant hyperthermia. Excessive phosphate administration from IV


Surgery_Schwartz

Surgery_Schwartz. that results in cell destruction, includ-ing rhabdomyolysis, tumor lysis syndrome, hemolysis, sepsis, severe hypothermia, and malignant hyperthermia. Excessive phosphate administration from IV hyperalimentation solutions or phosphorus-containing laxatives may also lead to elevated phosphate levels. Most cases of hyperphosphatemia are asymp-tomatic, but significant prolonged hyperphosphatemia can lead to metastatic deposition of soft tissue calcium-phosphorus complexes.Hypophosphatemia Hypophosphatemia can be due to a decrease in phosphorus intake, an intracellular shift of phospho-rus, or an increase in phosphorus excretion. Decreased GI uptake due to malabsorption or administration of phosphate binders and decreased dietary intake from malnutrition are causes of chronic hypophosphatemia. Most acute cases are due to an intracellular Brunicardi_Ch03_p0083-p0102.indd 9008/12/18 10:07 AM 91FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTCHAPTER 3shift of phosphorus in


Surgery_Schwartz

Surgery_Schwartz. Most acute cases are due to an intracellular Brunicardi_Ch03_p0083-p0102.indd 9008/12/18 10:07 AM 91FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTCHAPTER 3shift of phosphorus in association with respiratory alkalosis, insulin therapy, refeeding syndrome, and hungry bone syn-drome. Clinical manifestations of hypophosphatemia usually are absent until levels fall significantly. In general, symptoms are related to adverse effects on the oxygen availability of tissue and to a decrease in high-energy phosphates, and can be mani-fested as cardiac dysfunction or muscle weakness.Magnesium Abnormalities. Magnesium is the fourth most common mineral in the body and, like potassium, is found pri-marily in the intracellular compartments. Approximately one-half of the total body content of 2000 mEq is incorporated in bone and is slowly exchangeable. Of the fraction found in the extracellular space, one-third is bound to serum albumin. There-fore, the plasma level of magnesium may be a


Surgery_Schwartz

Surgery_Schwartz. 2000 mEq is incorporated in bone and is slowly exchangeable. Of the fraction found in the extracellular space, one-third is bound to serum albumin. There-fore, the plasma level of magnesium may be a poor indicator of total body stores in the presence of hypoalbuminemia. Mag-nesium should be replaced until levels are in the upper limit of normal. The normal dietary intake is approximately 20 mEq/d and is excreted in both the feces and urine. The kidneys have a remarkable ability to conserve magnesium, with renal excretion <1 mEq/d during magnesium deficiency.Hypermagnesemia Hypermagnesemia is rare but can be seen with severe renal insufficiency and parallel changes in potas-sium excretion. Magnesium-containing antacids and laxatives can produce toxic levels in patients with renal failure. Excess intake in conjunction with total parenteral nutrition (TPN), or, rarely, massive trauma, thermal injury, and severe acidosis, may be associated with symptomatic hypermagnesemia. Clini-cal


Surgery_Schwartz

Surgery_Schwartz. Excess intake in conjunction with total parenteral nutrition (TPN), or, rarely, massive trauma, thermal injury, and severe acidosis, may be associated with symptomatic hypermagnesemia. Clini-cal examination (see Table 3-6) may find nausea and vomit-ing; neuromuscular dysfunction with weakness, lethargy, and hyporeflexia; and impaired cardiac conduction leading to hypo-tension and arrest. ECG changes are similar to those seen with hyperkalemia and include increased PR interval, widened QRS complex, and elevated T waves.Hypomagnesemia Magnesium depletion is a common prob-lem in hospitalized patients, particularly in the critically ill.16 The kidney is primarily responsible for magnesium homeostasis through regulation by calcium/magnesium receptors on the renal tubular cells that respond to serum magnesium concentrations.17 Hypomagnesemia may result from alterations of intake, renal excretion, and pathologic losses. Poor intake may occur in cases of starvation, alcoholism, prolonged IV


Surgery_Schwartz

Surgery_Schwartz. serum magnesium concentrations.17 Hypomagnesemia may result from alterations of intake, renal excretion, and pathologic losses. Poor intake may occur in cases of starvation, alcoholism, prolonged IV fluid therapy, and TPN with inadequate supplementation of magnesium. Losses are seen in cases of increased renal excretion from alcohol abuse, diuretic use, administration of amphotericin B, and primary aldosteronism, as well as GI losses from diarrhea, malabsorp-tion, and acute pancreatitis. The magnesium ion is essential for proper function of many enzyme systems. Depletion is characterized by neuromuscular and central nervous system hyperactivity. Symptoms are similar to those of calcium defi-ciency, including hyperactive reflexes, muscle tremors, tetany, and positive Chvostek’s and Trousseau’s signs (see Table 3-6). Severe deficiencies can lead to delirium and seizures. A number of ECG changes also can occur and include prolonged QT and PR intervals, ST-segment depression, flattening


Surgery_Schwartz

Surgery_Schwartz. signs (see Table 3-6). Severe deficiencies can lead to delirium and seizures. A number of ECG changes also can occur and include prolonged QT and PR intervals, ST-segment depression, flattening or inversion of P waves, torsades de pointes, and arrhythmias. Hypomagnese-mia is important not only because of its direct effects on the nervous system but also because it can produce hypocalcemia and lead to persistent hypokalemia. When hypokalemia or hypo-calcemia coexists with hypomagnesemia, magnesium should be aggressively replaced to assist in restoring potassium or calcium homeostasis.Acid-Base BalanceAcid-Base Homeostasis. The pH of body fluids is maintained within a narrow range despite the ability of the kidneys to gen-erate large amounts of HCO3− and the normal large acid load produced as a by-product of metabolism. This endogenous acid load is efficiently neutralized by buffer systems and ultimately excreted by the lungs and kidneys.Important buffers include intracellular proteins


Surgery_Schwartz

Surgery_Schwartz. as a by-product of metabolism. This endogenous acid load is efficiently neutralized by buffer systems and ultimately excreted by the lungs and kidneys.Important buffers include intracellular proteins and phos-phates and the extracellular bicarbonate–carbonic acid system. Compensation for acid-base derangements can be by respiratory mechanisms (for metabolic derangements) or metabolic mecha-nisms (for respiratory derangements). Changes in ventilation in response to metabolic abnormalities are mediated by hydrogen-sensitive chemoreceptors found in the carotid body and brain stem. Acidosis stimulates the chemoreceptors to increase venti-lation, whereas alkalosis decreases the activity of the chemore-ceptors and thus decreases ventilation. The kidneys provide compensation for respiratory abnormalities by either increasing or decreasing bicarbonate reabsorption in response to respira-tory acidosis or alkalosis, respectively. Unlike the prompt change in ventilation that occurs with


Surgery_Schwartz

Surgery_Schwartz. abnormalities by either increasing or decreasing bicarbonate reabsorption in response to respira-tory acidosis or alkalosis, respectively. Unlike the prompt change in ventilation that occurs with metabolic abnormalities, the compensatory response in the kidneys to respiratory abnor-malities is delayed. Significant compensation may not begin for 6 hours and then may continue for several days. Because of this delayed compensatory response, respiratory acid-base derange-ments before renal compensation are classified as acute, whereas those persisting after renal compensation are categorized as chronic. The predicted compensatory changes in response to metabolic or respiratory derangements are listed in Table 3-7.18 If the predicted change in pH is exceeded, then a mixed acid-base abnormality may be present (Table 3-8).Metabolic DerangementsMetabolic Acidosis. Metabolic acidosis results from an increased intake of acids, an increased generation of acids, or an increased loss of


Surgery_Schwartz

Surgery_Schwartz. may be present (Table 3-8).Metabolic DerangementsMetabolic Acidosis. Metabolic acidosis results from an increased intake of acids, an increased generation of acids, or an increased loss of bicarbonate (Table 3-9). The body responds by several mechanisms, including producing buffers (extracellular bicarbonate and intracellular buffers from bone and muscle), increasing ventilation (Kussmaul’s respirations), and increas-ing renal reabsorption and generation of bicarbonate. The kid-ney also will increase secretion of hydrogen and thus increase urinary excretion of NH4+ (H+ + NH3+ = NH4+). Evaluation of a patient with a low serum bicarbonate level and metabolic 4Table 3-7 Predicted changes in acid-base disordersDISORDERPREDICTED CHANGEMetabolic Metabolic acidosis Metabolic alkalosisRespiratory Acute respiratory acidosis Chronic respiratory acidosis Acute respiratory alkalosis Chronic respiratory alkalosisPco2 = 1.5 × HCO3− + 8Pco2 = 0.7 × HCO3− + 21Δ pH = (Pco2 – 40) × 0.008Δ pH =


Surgery_Schwartz

Surgery_Schwartz. respiratory acidosis Chronic respiratory acidosis Acute respiratory alkalosis Chronic respiratory alkalosisPco2 = 1.5 × HCO3− + 8Pco2 = 0.7 × HCO3− + 21Δ pH = (Pco2 – 40) × 0.008Δ pH = (Pco2 – 40) × 0.003 Δ pH = (40 – Pco2) × 0.008Δ pH = (40 – Pco2) × 0.017Pco2 = partial pressure of carbon dioxide.Brunicardi_Ch03_p0083-p0102.indd 9108/12/18 10:07 AM 92BASIC CONSIDERATIONSPART Iacidosis includes determination of the anion gap (AG), an index of unmeasured anions.AG = (Na) – (Cl + HCO3)The normal AG is <12 mmol/L and is due primarily to the albumin effect, so that the estimated AG must be adjusted for albumin (hypoalbuminemia reduces the AG).19Corrected AG = actual AG – (2.5[4.5 – albumin])Metabolic acidosis with an increased AG occurs either from ingestion of exogenous acid such as from ethylene gly-col, salicylates, or methanol, or from increased endogenous acid production of the following:• β-Hydroxybutyrate and acetoacetate in ketoacidosis• Lactate in lactic acidosis• Organic


Surgery_Schwartz

Surgery_Schwartz. ethylene gly-col, salicylates, or methanol, or from increased endogenous acid production of the following:• β-Hydroxybutyrate and acetoacetate in ketoacidosis• Lactate in lactic acidosis• Organic acids in renal insufficiencyA common cause of severe metabolic acidosis in surgi-cal patients is lactic acidosis. In circulatory shock, lactate is produced in the presence of hypoxia from inadequate tissue perfusion. The treatment is to restore perfusion with volume resuscitation rather than to attempt to correct the abnormality with exogenous bicarbonate. With adequate perfusion, the lactic acid is rapidly metabolized by the liver, and the pH level returns to normal. In clinical studies of lactic acidosis and ketoacidosis, the administration of bicarbonate has not reduced morbidity or mortality or improved cellular function.20 Administered bicar-bonate can combine with the excess hydrogen ions to form car-bonic acid; this is then converted to CO2 and water, which thus raises the partial


Surgery_Schwartz

Surgery_Schwartz. or improved cellular function.20 Administered bicar-bonate can combine with the excess hydrogen ions to form car-bonic acid; this is then converted to CO2 and water, which thus raises the partial pressure of CO2 (Pco2). This hypercarbia could compound ventilation abnormalities in patients with underlying acute respiratory distress syndrome. This CO2 can diffuse into cells, but bicarbonate remains extracellular, which thus worsens intracellular acidosis. Clinically, lactate levels may not be useful in directing resuscitation, although lactate levels may be higher in nonsurvivors of serious injury.21Metabolic acidosis with a normal AG results from exog-enous acid administration (HCl or NH4+), from loss of bicar-bonate due to GI disorders such as diarrhea and fistulas or ureterosigmoidostomy, or from renal losses. In these settings, the bicarbonate loss is accompanied by a gain of chloride; thus, the AG remains unchanged. To determine whether the loss of bicarbonate has a renal cause,


Surgery_Schwartz

Surgery_Schwartz. or from renal losses. In these settings, the bicarbonate loss is accompanied by a gain of chloride; thus, the AG remains unchanged. To determine whether the loss of bicarbonate has a renal cause, the urinary (NH4+) can be mea-sured. A low urinary (NH4+) in the face of hyperchloremic acidosis would indicate that the kidney is the site of loss, and evaluation for renal tubular acidosis should be undertaken. Prox-imal renal tubular acidosis results from decreased tubular reab-sorption of HCO3−, whereas distal renal tubular acidosis results from decreased acid excretion. The carbonic anhydrase inhibitor acetazolamide also causes bicarbonate loss from the kidneys.Metabolic Alkalosis Normal acid-base homeostasis prevents metabolic alkalosis from developing unless both an increase in bicarbonate generation and impaired renal excretion of bicar-bonate occur (Table 3-10). Metabolic alkalosis results from the loss of fixed acids or the gain of bicarbonate and is worsened by potassium depletion.


Surgery_Schwartz

Surgery_Schwartz. generation and impaired renal excretion of bicar-bonate occur (Table 3-10). Metabolic alkalosis results from the loss of fixed acids or the gain of bicarbonate and is worsened by potassium depletion. The majority of patients also will have hypokalemia because extracellular potassium ions exchange with intracellular hydrogen ions and allow the hydrogen ions to buffer excess HCO3–. Hypochloremic and hypokalemic meta-bolic alkalosis can occur from isolated loss of gastric contents in infants with pyloric stenosis or adults with duodenal ulcer disease. Unlike vomiting associated with an open pylorus, which involves a loss of gastric as well as pancreatic, biliary, Table 3-9 Etiology of metabolic acidosisIncreased Anion Gap Metabolic AcidosisExogenous acid ingestion Ethylene glycol Salicylate MethanolEndogenous acid production Ketoacidosis Lactic acidosis Renal insufficiencyNormal Anion GapAcid administration (HCl)Loss of bicarbonateGI losses (diarrhea, fistulas)UreterosigmoidostomyRenal


Surgery_Schwartz

Surgery_Schwartz. acid production Ketoacidosis Lactic acidosis Renal insufficiencyNormal Anion GapAcid administration (HCl)Loss of bicarbonateGI losses (diarrhea, fistulas)UreterosigmoidostomyRenal tubular acidosisCarbonic anhydrase inhibitorTable 3-8 Respiratory and metabolic components of acid-base disorders ACUTE UNCOMPENSATEDCHRONIC (PARTIALLY COMPENSATED)TYPE OF ACID-BASE DISORDERpHPco2 (RESPIRATORY COMPONENT)PLASMA HCO3−a (METABOLIC COMPONENT)pHPco2 (RESPIRATORY COMPONENT)PLASMA HCO3−a (METABOLIC COMPONENT)Respiratory acidosis↓↓↑↑N↓↑↑↑Respiratory alkalosis↑↑↓↓N↑↓↓↓Metabolic acidosis↓↓N↓↓↓↓↓Metabolic alkalosis↑↑N↑↑↑↑↑aMeasured as standard bicarbonate, whole blood buffer base, CO2 content, or CO2 combining power. The base excess value is positive when the standard bicarbonate is above normal and negative when the standard bicarbonate is below normal.N = normal; Pco2 = partial pressure of carbon dioxide.Brunicardi_Ch03_p0083-p0102.indd 9208/12/18 10:07 AM 93FLUID AND ELECTROLYTE MANAGEMENT OF


Surgery_Schwartz

Surgery_Schwartz. when the standard bicarbonate is below normal.N = normal; Pco2 = partial pressure of carbon dioxide.Brunicardi_Ch03_p0083-p0102.indd 9208/12/18 10:07 AM 93FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTCHAPTER 3and intestinal secretions, vomiting with an obstructed pylorus results only in the loss of gastric fluid, which is high in chloride and hydrogen, and therefore results in a hypochloremic alkalo-sis. Initially, the urinary bicarbonate level is high in compensa-tion for the alkalosis. Hydrogen ion reabsorption also ensues, with an accompanied potassium ion excretion. In response to the associated volume deficit, aldosterone-mediated sodium reabsorption increases potassium excretion. The resulting hypo-kalemia leads to the excretion of hydrogen ions in the face of alkalosis, a paradoxic aciduria. Treatment includes replacement of the volume deficit with isotonic saline and then potassium replacement once adequate urine output is achieved.Respiratory


Surgery_Schwartz

Surgery_Schwartz. face of alkalosis, a paradoxic aciduria. Treatment includes replacement of the volume deficit with isotonic saline and then potassium replacement once adequate urine output is achieved.Respiratory Derangements. Under normal circumstances, blood Pco2 is tightly maintained by alveolar ventilation, con-trolled by the respiratory centers in the pons and medulla oblongata.Respiratory Acidosis Respiratory acidosis is associated with the retention of CO2 secondary to decreased alveolar ventila-tion. The principal causes are listed in Table 3-11. Because compensation is primarily a renal mechanism, it is a delayed response. Treatment of acute respiratory acidosis is directed at the underlying cause. Measures to ensure adequate ventila-tion are also initiated. This may entail patient-initiated volume expansion using noninvasive bilevel positive airway pressure or may require endotracheal intubation to increase minute ven-tilation. In the chronic form of respiratory acidosis, the partial


Surgery_Schwartz

Surgery_Schwartz. volume expansion using noninvasive bilevel positive airway pressure or may require endotracheal intubation to increase minute ven-tilation. In the chronic form of respiratory acidosis, the partial pressure of arterial CO2 remains elevated, and the bicarbonate concentration rises slowly as renal compensation occurs.Respiratory Alkalosis In the surgical patient, most cases of respiratory alkalosis are acute and secondary to alveolar hyper-ventilation. Causes include pain, anxiety, and neurologic dis-orders, including central nervous system injury and assisted ventilation. Drugs such as salicylates, fever, gram-negative bacteremia, thyrotoxicosis, and hypoxemia are other possibili-ties. Acute hypocapnia can cause an uptake of potassium and phosphate into cells and increased binding of calcium to albu-min, leading to symptomatic hypokalemia, hypophosphatemia, and hypocalcemia with subsequent arrhythmias, paresthesias, muscle cramps, and seizures. Treatment should be directed at the


Surgery_Schwartz

Surgery_Schwartz. calcium to albu-min, leading to symptomatic hypokalemia, hypophosphatemia, and hypocalcemia with subsequent arrhythmias, paresthesias, muscle cramps, and seizures. Treatment should be directed at the underlying cause, but direct treatment of the hyperventila-tion using controlled ventilation may also be required.FLUID AND ELECTROLYTE THERAPYParenteral SolutionsA number of commercially available electrolyte solutions are available for parenteral administration. The most commonly used solutions are listed in Table 3-12. The type of fluid admin-istered depends on the patient’s volume status and the type of concentration or compositional abnormality present. Plasma-Lyte, lactated Ringer’s solution, and normal saline are consid-ered isotonic and are useful in replacing GI losses and correcting extracellular volume deficits. Lactated Ringer’s is slightly hypotonic in that it contains 130 mEq of lactate. Lactate is used rather than bicarbonate because it is more stable in IV fluids during


Surgery_Schwartz

Surgery_Schwartz. extracellular volume deficits. Lactated Ringer’s is slightly hypotonic in that it contains 130 mEq of lactate. Lactate is used rather than bicarbonate because it is more stable in IV fluids during storage. It is converted into bicarbonate by the liver after infusion, even in the face of hemorrhagic shock.Sodium chloride is mildly hypertonic, containing 154 mEq of sodium that is balanced by 154 mEq of chloride. The high chloride concentration imposes a significant chloride load on the kidneys and may lead to a hyperchloremic metabolic acido-sis. Sodium chloride is an ideal solution, however, for correcting volume deficits associated with hyponatremia, hypochloremia, and metabolic alkalosis.Plasma-Lyte is the crystalloid preparation that most closely resembles the electrolyte composition of human plasma. In addi-tion to the favorable, isotonic electrolyte composition, Plasma-Lyte contains a number of additional buffers that create a favorable profile for addressing acidosis.22 These


Surgery_Schwartz

Surgery_Schwartz. of human plasma. In addi-tion to the favorable, isotonic electrolyte composition, Plasma-Lyte contains a number of additional buffers that create a favorable profile for addressing acidosis.22 These characteristics have resulted in Plasma-Lyte emerging as one of the most popular isotonic fluids for use in surgery. It should be noted that Plasma-Lyte contains small quantities of potassium; although the likeli-hood of inducing hyperkalemia is very low, care should be taken when using Plasma-Lyte in patients at risk for renal impairment. The less concentrated sodium solutions, such as 0.45% sodium chloride, are useful for replacement of ongoing GI losses as well as for maintenance fluid therapy in the post-operative period. This solution provides sufficient free water for insensible losses and enough sodium to aid the kidneys in adjustment of serum sodium levels. The addition of 5% dextrose Table 3-10 Etiology of metabolic alkalosisIncreased bicarbonate generation1. Chloride losing


Surgery_Schwartz

Surgery_Schwartz. and enough sodium to aid the kidneys in adjustment of serum sodium levels. The addition of 5% dextrose Table 3-10 Etiology of metabolic alkalosisIncreased bicarbonate generation1. Chloride losing (urinary chloride >20 mEq/L)Mineralocorticoid excessProfound potassium depletion2. Chloride sparing (urinary chloride <20 mEq/L)Loss from gastric secretions (emesis or nasogastric suction)Diuretics3. Excess administration of alkaliAcetate in parenteral nutritionCitrate in blood transfusionsAntacidsBicarbonateMilk-alkali syndromeImpaired bicarbonate excretion1. Decreased glomerular filtration2. Increased bicarbonate reabsorption (hypercarbia or potassium depletion)Table 3-11Etiology of respiratory acidosis: hypoventilationNarcoticsCentral nervous system injuryPulmonary: significant Secretions Atelectasis Mucus plug Pneumonia Pleural effusionPain from abdominal or thoracic injuries or incisionsLimited diaphragmatic excursion from intra-abdominal pathology Abdominal distention Abdominal


Surgery_Schwartz

Surgery_Schwartz. plug Pneumonia Pleural effusionPain from abdominal or thoracic injuries or incisionsLimited diaphragmatic excursion from intra-abdominal pathology Abdominal distention Abdominal compartment syndrome AscitesBrunicardi_Ch03_p0083-p0102.indd 9308/12/18 10:07 AM 94BASIC CONSIDERATIONSPART I(50 g of dextrose per liter) supplies 200 kcal/L, and dextrose is always added to solutions containing <0.45% sodium chloride to maintain osmolality and thus prevent the lysis of red blood cells that may occur with rapid infusion of hypotonic fluids. The addition of potassium is useful once adequate renal function and urine output are established.Alternative Resuscitative FluidsA number of alternative solutions for volume expansion and resuscitation are available (Table 3-13).23 Hypertonic saline solutions (3.5% and 5%) are used for correction of severe sodium deficits and are discussed elsewhere in this chap-ter. Hypertonic saline (7.5%) has been used as a treatment modality in patients with closed


Surgery_Schwartz

Surgery_Schwartz. (3.5% and 5%) are used for correction of severe sodium deficits and are discussed elsewhere in this chap-ter. Hypertonic saline (7.5%) has been used as a treatment modality in patients with closed head injuries. It has been shown to increase cerebral perfusion and decrease intracranial pressure, thus decreasing brain edema.24 However, there have also been concerns about increased bleeding because hypertonic saline is an arteriolar vasodilator. A recent meta-analysis of hypertonic saline in severe traumatic brain injury revealed that, in a total of 11 eligible studies, there was no mortality benefit associated with hypertonic saline compared to other solutions.25 Colloids also are used in surgical patients, and their effectiveness as vol-ume expanders compared with isotonic crystalloids has long been debated. Due to their molecular weight, they are confined to the intravascular space, and their infusion results in more effi-cient transient plasma volume expansion. However, under


Surgery_Schwartz

Surgery_Schwartz. has long been debated. Due to their molecular weight, they are confined to the intravascular space, and their infusion results in more effi-cient transient plasma volume expansion. However, under con-ditions of severe hemorrhagic shock, capillary membrane permeability increases; this permeability permits colloids to enter the interstitial space, which can worsen edema and impair tissue oxygenation. Four major types of colloids are available—albumin, dextrans, hetastarch, and gelatins—and are described by their molecular weight and size in Table 3-13. In a large randomized trial of patients admitted to an intensive care unit with hypovolemic shock, administration of colloid showed no improvement in mortality at 30 days as compared to crystalloid resuscitation.26 Interestingly, there was a suggestion of improve-ment of 90-day mortality and more days alive without mechani-cal ventilation in patients receiving colloid; however, these were not trial primary endpoints and were considered


Surgery_Schwartz

Surgery_Schwartz. a suggestion of improve-ment of 90-day mortality and more days alive without mechani-cal ventilation in patients receiving colloid; however, these were not trial primary endpoints and were considered exploratory. Furthermore, a Cochrane Database systematic review on the topic concluded that there is no available evidence from ran-domized trials to support colloid use over crystalloid to reduce the risk of death following trauma, burns, or surgery.27 Colloids are markedly more expensive than crystalloids, and certain col-loids, such as hydroxyethyl starch, have been associated with increased morbidity including the need for renal replacement therapy.28 Taken together, the use of colloid for resuscitation of critically ill and surgical patients has limited application.Correction of Life-Threatening Electrolyte AbnormalitiesSodium Hypernatremia Treatment of hypernatremia usually consists of treatment of the associated water deficit. In hypovolemic patients, volume should be restored with


Surgery_Schwartz

Surgery_Schwartz. Electrolyte AbnormalitiesSodium Hypernatremia Treatment of hypernatremia usually consists of treatment of the associated water deficit. In hypovolemic patients, volume should be restored with normal saline before the concentration abnormality is addressed. Once adequate volume has been achieved, the water deficit is replaced using a hypotonic fluid such as 5% dextrose, 5% dextrose in onequarter normal saline, or enterally administered water. The for-mula used to estimate the amount of water required to correct hypernatremia is as follows:Waterdeficit(L)serumsodium140=−×140TBWEstimate TBW as 50% of lean body mass in men and 40% in women5Table 3-12 Electrolyte solutions for parenteral administration ELECTROLYTE COMPOSITION (mEq/L)SOLUTIONNaClKHCO3−CaMgmOsmExtracellular fluid14210342753280–310Lactated Ringer’s1301094283 2730.9% Sodium chloride154154 308D5 0.45% Sodium chloride7777 407D5W 2533% Sodium chloride513513 1026Plasma-Lyte14098527 3295D5 = 5% dextrose; D5W = 5%


Surgery_Schwartz

Surgery_Schwartz. Ringer’s1301094283 2730.9% Sodium chloride154154 308D5 0.45% Sodium chloride7777 407D5W 2533% Sodium chloride513513 1026Plasma-Lyte14098527 3295D5 = 5% dextrose; D5W = 5% dextrose in water.Table 3-13 Alternative resuscitative fluidsSOLUTIONMOLECULAR WEIGHTOSMOLALITY (mOsm/L)SODIUM (mEq/L)Hypertonic saline (7.5%)—25651283Albumin 5%70,000300130–160Albumin 25%70,0001500130–160Dextran 4040,000308154Dextran 7070,000308154Hetastarch450,000310154Hextend670,000307143Gelofusine30,000NA154NA = not available.Brunicardi_Ch03_p0083-p0102.indd 9408/12/18 10:07 AM 95FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTCHAPTER 3The rate of fluid administration should be titrated to achieve a decrease in serum sodium concentration of no more than 1 mEq/h and 12 mEq/d for the treatment of acute symp-tomatic hypernatremia. Even slower correction should be under-taken for chronic hypernatremia (0.7 mEq/h) because overly rapid correction can lead to cerebral edema and herniation. The


Surgery_Schwartz

Surgery_Schwartz. of acute symp-tomatic hypernatremia. Even slower correction should be under-taken for chronic hypernatremia (0.7 mEq/h) because overly rapid correction can lead to cerebral edema and herniation. The type of fluid used depends on the severity and ease of correc-tion. Oral or enteral replacement is acceptable in most cases, or IV replacement with halfor quarter-normal saline can be used. Caution also should be exercised when using 5% dextrose in water to avoid overly rapid correction. Frequent neurologic evaluation as well as frequent evaluation of serum sodium levels also should be performed. Hypernatremia is less common than hyponatremia, but has a worse prognosis, and is an independent predictor of mortality in critical illness.29Hyponatremia Most cases of hyponatremia can be treated by free water restriction and, if severe, the administration of sodium. In patients with normal renal function, symptomatic hyponatremia usually does not occur until the serum sodium level is ≤120 mEq/L.


Surgery_Schwartz

Surgery_Schwartz. water restriction and, if severe, the administration of sodium. In patients with normal renal function, symptomatic hyponatremia usually does not occur until the serum sodium level is ≤120 mEq/L. If neurologic symptoms are present, 3% normal saline should be used to increase the sodium by no more than 1 mEq/L per hour until the serum sodium level reaches 130 mEq/L or neurologic symptoms are improved. Correction of asymptomatic hyponatremia should increase the sodium level by no more than 0.5 mEq/L per hour to a maxi-mum increase of 12 mEq/L per day, and even more slowly in chronic hyponatremia. The rapid correction of hyponatremia can lead to pontine myelinolysis,30 with seizures, weakness, paresis, akinetic movements, and unresponsiveness, and may result in permanent brain damage and death. Serial magnetic resonance imaging may be necessary to confirm the diagnosis.31Potassium Hyperkalemia Treatment options for symptomatic hyperka-lemia are listed in Table 3-14. The goals of therapy


Surgery_Schwartz

Surgery_Schwartz. Serial magnetic resonance imaging may be necessary to confirm the diagnosis.31Potassium Hyperkalemia Treatment options for symptomatic hyperka-lemia are listed in Table 3-14. The goals of therapy include reducing the total body potassium, shifting potassium from the extracellular to the intracellular space, and protecting the cells from the effects of increased potassium. For all patients, exogenous sources of potassium should be removed, including potassium supplementation in IV fluids and enteral and paren-teral solutions. Potassium can be removed from the body using a cation-exchange resin such as Kayexalate that binds potas-sium in exchange for sodium. It can be administered either orally, in alert patients, or rectally. Immediate measures also should include attempts to shift potassium intracellularly with glucose and bicarbonate infusion. Nebulized albuterol (10 to 20 mg) may also be used. Use of glucose alone will cause a rise in insulin secretion, but in the acutely ill, this


Surgery_Schwartz

Surgery_Schwartz. intracellularly with glucose and bicarbonate infusion. Nebulized albuterol (10 to 20 mg) may also be used. Use of glucose alone will cause a rise in insulin secretion, but in the acutely ill, this response may be blunted, and therefore both glucose and insulin may be necessary. Circulatory overload and hypernatremia may result from the administration of Kayexalate and bicarbonate, so care should be exercised when administering these agents to patients with fragile cardiac function. When ECG changes are present, calcium chloride or calcium gluconate (5 to 10 mL of 10% solution) should be administered immediately to counteract the myocardial effects of hyperkalemia. Calcium infusion should be used cautiously in patients receiving digitalis because digitalis toxicity may be precipitated. All of the aforementioned mea-sures are temporary, lasting from 1 to approximately 4 hours. Dialysis should be considered in severe hyperkalemia when conservative measures fail.Hypokalemia Treatment for


Surgery_Schwartz

Surgery_Schwartz. of the aforementioned mea-sures are temporary, lasting from 1 to approximately 4 hours. Dialysis should be considered in severe hyperkalemia when conservative measures fail.Hypokalemia Treatment for hypokalemia consists of potas-sium repletion, the rate of which is determined by the symptoms (Table 3-15). Oral repletion is adequate for mild, asymptomatic hypokalemia. If IV repletion is required, usually no more than 10 mEq/h is advisable in an unmonitored setting. This amount can be increased to 40 mEq/h when accompanied by continu-ous ECG monitoring, and even more in the case of imminent cardiac arrest from a malignant arrhythmia-associated hypoka-lemia. Caution should be exercised when oliguria or impaired renal function is coexistent.Calcium Hypercalcemia Treatment is required when hypercalcemia is symptomatic, which usually occurs when the serum level exceeds 12 mg/dL. The critical level for serum calcium is 15 mg/dL, when symptoms noted earlier may rapidly progress to death. The


Surgery_Schwartz

Surgery_Schwartz. is symptomatic, which usually occurs when the serum level exceeds 12 mg/dL. The critical level for serum calcium is 15 mg/dL, when symptoms noted earlier may rapidly progress to death. The initial treatment is aimed at repleting the associated volume deficit and then inducing a brisk diuresis with normal saline. Treatment of hypercalcemia associated with malignancies is discussed later in this chapter.Hypocalcemia Asymptomatic hypocalcemia can be treated with oral or IV calcium (see Table 3-15). Acute symptomatic hypocalcemia should be treated with IV 10% calcium gluconate to achieve a serum concentration of 7 to 9 mg/dL. Associated deficits in magnesium, potassium, and pH must also be cor-rected. Hypocalcemia will be refractory to treatment if coex-isting hypomagnesemia is not corrected first. Routine calcium supplementation is no longer recommended in association with massive blood transfusions.32Phosphorus Hyperphosphatemia Phosphate binders such as sucralfate or


Surgery_Schwartz

Surgery_Schwartz. is not corrected first. Routine calcium supplementation is no longer recommended in association with massive blood transfusions.32Phosphorus Hyperphosphatemia Phosphate binders such as sucralfate or aluminum-containing antacids can be used to lower serum phosphorus levels. Calcium acetate tablets also are useful when hypocalcemia is simultaneously present. Dialysis usually is reserved for patients with renal failure.Hypophosphatemia Depending on the level of depletion and tolerance to oral supplementation, a number of enteral and par-enteral repletion strategies are effective for the treatment of hypophosphatemia (see Table 3-15).Magnesium Hypermagnesemia Treatment for hypermagnesemia consists of measures to eliminate exogenous sources of magnesium, Table 3-14Treatment of symptomatic hyperkalemiaPotassium removal Kayexalate Oral administration is 15–30 g in 50–100 mL of 20% sorbitol Rectal administration is 50 g in 200 mL of 20% sorbitol DialysisShift potassium Glucose 1 ampule of


Surgery_Schwartz

Surgery_Schwartz. removal Kayexalate Oral administration is 15–30 g in 50–100 mL of 20% sorbitol Rectal administration is 50 g in 200 mL of 20% sorbitol DialysisShift potassium Glucose 1 ampule of D50 and regular insulin 5–10 units IV Bicarbonate 1 ampule IVCounteract cardiac effects Calcium gluconate 5–10 mL of 10% solutionD50 = 50% dextrose.Brunicardi_Ch03_p0083-p0102.indd 9508/12/18 10:07 AM 96BASIC CONSIDERATIONSPART ITable 3-15Electrolyte replacement therapy protocolPotassiumSerum potassium level <4.0 mEq/L: Asymptomatic, tolerating enteral nutrition: KCl 40 mEq per enteral access × 1 dose Asymptomatic, not tolerating enteral nutrition: KCl 20 mEq IV q2h × 2 doses Symptomatic: KCl 20 mEq IV q1h × 4 doses Recheck potassium level 2 h after end of infusion; if <3.5 mEq/L and asymptomatic, replace as per above protocolMagnesiumMagnesium level 1.0–1.8 mEq/L: Magnesium sulfate 0.5 mEq/kg in normal saline 250 mL infused IV over 24 h × 3 d Recheck magnesium level in 3 dMagnesium level <1.0


Surgery_Schwartz

Surgery_Schwartz. replace as per above protocolMagnesiumMagnesium level 1.0–1.8 mEq/L: Magnesium sulfate 0.5 mEq/kg in normal saline 250 mL infused IV over 24 h × 3 d Recheck magnesium level in 3 dMagnesium level <1.0 mEq/L: Magnesium sulfate 1 mEq/kg in normal saline 250 mL infused IV over 24 h × 1 d, then 0.5 mEq/kg in normal saline 250 mL infused IV over 24 h × 2 d Recheck magnesium level in 3 dIf patient has gastric access and needs a bowel regimen: Milk of magnesia 15 mL (approximately 49 mEq magnesium) q24h per gastric tube; hold for diarrheaCalciumIonized calcium level <4.0 mg/dL: With gastric access and tolerating enteral nutrition: Calcium carbonate suspension 1250 mg/5 mL q6h per gastric access; recheck ionized calcium level in 3 d Without gastric access or not tolerating enteral nutrition: Calcium gluconate 2 g IV over 1 h × 1 dose; recheck ionized calcium level in 3 dPhosphatePhosphate level 1.0–2.5 mg/dL: Tolerating enteral nutrition: Neutra-Phos 2 packets q6h per gastric tube or


Surgery_Schwartz

Surgery_Schwartz. Calcium gluconate 2 g IV over 1 h × 1 dose; recheck ionized calcium level in 3 dPhosphatePhosphate level 1.0–2.5 mg/dL: Tolerating enteral nutrition: Neutra-Phos 2 packets q6h per gastric tube or feeding tube No enteral nutrition: KPHO4 or NaPO4 0.15 mmol/kg IV over 6 h × 1 dose Recheck phosphate level in 3 dPhosphate level <1.0 mg/dL: Tolerating enteral nutrition: KPHO4 or NaPO4 0.25 mmol/kg over 6 h × 1 dose Recheck phosphate level 4 h after end of infusion; if <2.5 mg/dL, begin Neutra-Phos 2 packets q6h Not tolerating enteral nutrition: KPHO4 or NaPO4 0.25 mmol/kg (LBW) over 6 h × 1 dose; recheck phosphate level 4 h after end of infusion; if <2.5 mg/dL, then KPHO4 or NaPO4 0.15 mmol/kg (LBW) IV over 6 h × 1 dose3 mmol KPHO4 = 3 mmol Phos and 4.4 mEq K+ = 1 mL3 mmol NaPO4 = 3 mmol Phos and 4 mEq Na+ = 1 mLNeutra-Phos 1 packet = 8 mmol Phos, 7 mEq K+, 7 mEq Na+Use patient’s lean body weight (LBW) in kilograms for all calculations.Disregard protocol if patient has renal failure,


Surgery_Schwartz

Surgery_Schwartz. Phos and 4 mEq Na+ = 1 mLNeutra-Phos 1 packet = 8 mmol Phos, 7 mEq K+, 7 mEq Na+Use patient’s lean body weight (LBW) in kilograms for all calculations.Disregard protocol if patient has renal failure, is on dialysis, or has a creatinine clearance <30 mL/min.correct concurrent volume deficits, and correct acidosis if present. To manage acute symptoms, calcium chloride (5 to 10 mL) should be administered to immediately antagonize the cardiovascular effects. If elevated levels or symptoms persist, hemodialysis may be necessary.Hypomagnesemia Correction of magnesium depletion can be oral if asymptomatic and mild. Otherwise, IV repletion is indicated and depends on severity (see Table 3-15) and clini-cal symptoms. For those with severe deficits (<1.0 mEq/L) or those who are symptomatic, 1 to 2 g of magnesium sulfate may be administered IV over 15 minutes. Under ECG monitoring, it may be given over 2 minutes if necessary to correct torsades de pointes (irregular ventricular rhythm). Caution


Surgery_Schwartz

Surgery_Schwartz. g of magnesium sulfate may be administered IV over 15 minutes. Under ECG monitoring, it may be given over 2 minutes if necessary to correct torsades de pointes (irregular ventricular rhythm). Caution should be taken when giving large amounts of magnesium because magnesium toxicity may develop. The simultaneous administration of cal-cium gluconate will counteract the adverse side effects of a rap-idly rising magnesium level and correct hypocalcemia, which is frequently associated with hypomagnesemia.Preoperative Fluid TherapyThe administration of maintenance fluids should be all that is required in an otherwise healthy individual who may be under orders to receive nothing by mouth for some period before the time of surgery. This does not, however, include replenishment of a preexisting deficit or ongoing fluid losses. The following is a frequently used formula for calculating the volume of mainte-nance fluids in the absence of preexisting abnormalities:For the first 0–10 kgFor the next


Surgery_Schwartz

Surgery_Schwartz. or ongoing fluid losses. The following is a frequently used formula for calculating the volume of mainte-nance fluids in the absence of preexisting abnormalities:For the first 0–10 kgFor the next 10–20 kgFor weight >20 kgGive 100 mL/kg per dayGive an additional 50 mL/kg per dayGive an additional 20 mL/kg per dayFor example, a 60-kg female would receive a total of 2300 mL of fluid daily: 1000 mL for the first 10 kg of body Brunicardi_Ch03_p0083-p0102.indd 9608/12/18 10:07 AM 97FLUID AND ELECTROLYTE MANAGEMENT OF THE SURGICAL PATIENTCHAPTER 3weight (10 kg × 100 mL/kg per day), 500 mL for the next 20 kg (10 kg × 50 mL/kg per day), and 800 mL for the last 40 kg (40 kg × 20 mL/kg per day).An alternative approach is to replace the calculated daily water losses in urine, stool, and insensible loss with a hypotonic saline solution rather than water alone, which allows the kid-ney some sodium excess to adjust for concentration. Although there should be no “routine” maintenance fluid


Surgery_Schwartz

Surgery_Schwartz. loss with a hypotonic saline solution rather than water alone, which allows the kid-ney some sodium excess to adjust for concentration. Although there should be no “routine” maintenance fluid orders, both of these methods would yield an appropriate choice of 5% dex-trose in 0.45% sodium chloride at 100 mL/h as initial therapy, with potassium added for patients with normal renal function. However, many surgical patients have volume and/or electrolyte abnormalities associated with their surgical disease. Preopera-tive evaluation of a patient’s volume status and preexisting elec-trolyte abnormalities is an important part of overall preoperative assessment and care. Volume deficits should be considered in patients who have obvious GI losses, such as through emesis or diarrhea, as well as in patients with poor oral intake second-ary to their disease. Less obvious are those fluid losses known as third-space or nonfunctional ECF losses that occur with GI obstruction, peritoneal or bowel


Surgery_Schwartz

Surgery_Schwartz. in patients with poor oral intake second-ary to their disease. Less obvious are those fluid losses known as third-space or nonfunctional ECF losses that occur with GI obstruction, peritoneal or bowel inflammation, ascites, crush injuries, burns, and severe soft tissue infections such as nec-rotizing fasciitis. The diagnosis of an acute volume deficit is primarily clinical (see Table 3-2), although the physical signs may vary with the duration of the deficit. Cardiovascular signs of tachycardia and orthostasis predominate with acute volume loss, usually accompanied by oliguria and hemoconcentration. Acute volume deficits should be corrected as much as possible before the time of operation.Once a volume deficit is diagnosed, prompt fluid replace-ment should be instituted, usually with an isotonic crystalloid, depending on the measured serum electrolyte values. Patients with cardiovascular signs of volume deficit should receive a bolus of 1 to 2 L of isotonic fluid followed by a


Surgery_Schwartz

Surgery_Schwartz. an isotonic crystalloid, depending on the measured serum electrolyte values. Patients with cardiovascular signs of volume deficit should receive a bolus of 1 to 2 L of isotonic fluid followed by a continuous infu-sion. Close monitoring during this period is imperative. Resus-citation should be guided by the reversal of the signs of volume deficit, such as restoration of acceptable values for vital signs, maintenance of adequate urine output (0.5 to 1 mL/kg per hour in an adult), and correction of base deficit. Patients whose vol-ume deficit is not corrected after this initial volume challenge and those with impaired renal function and the elderly should be considered for more intensive monitoring in an intensive care unit setting. In these patients, early invasive monitoring of cen-tral venous pressure or cardiac output may be necessary.If symptomatic electrolyte abnormalities accompany vol-ume deficit, the abnormality should be corrected to the point that the acute symptom is


Surgery_Schwartz

Surgery_Schwartz. venous pressure or cardiac output may be necessary.If symptomatic electrolyte abnormalities accompany vol-ume deficit, the abnormality should be corrected to the point that the acute symptom is relieved before surgical interven-tion. For correction of severe hypernatremia associated with a volume deficit, an unsafe rapid fall in extracellular osmolarity from 5% dextrose infusion is avoided by slowly correcting the hypernatremia with 0.45% saline or even lactated Ringer’s solu-tion rather than 5% dextrose alone. This will safely and slowly correct the hypernatremia while also correcting the associated volume deficit.Intraoperative Fluid TherapyWith the induction of anesthesia, compensatory mechanisms are lost, and hypotension will develop if volume deficits are not appropriately corrected before the time of surgery. Hemody-namic instability during anesthesia is best avoided by correct-ing known fluid losses, replacing ongoing losses, and providing adequate maintenance fluid therapy


Surgery_Schwartz

Surgery_Schwartz. before the time of surgery. Hemody-namic instability during anesthesia is best avoided by correct-ing known fluid losses, replacing ongoing losses, and providing adequate maintenance fluid therapy preoperatively. In addition to measured blood loss, major open abdominal surgeries are associated with continued extracellular losses in the form of bowel wall edema, peritoneal fluid, and the wound edema dur-ing surgery. Large soft tissue wounds, complex fractures with associated soft tissue injury, and burns are all associated with additional third-space losses that must be considered in the operating room. These represent distributional shifts, in that the functional volume of ECF is reduced but fluid is not externally lost from the body. These functional losses have been referred to as parasitic losses, sequestration, or third-space edema because the lost volume no longer participates in the normal functions of the ECF.Until the 1960s saline solutions were withheld during sur-gery.


Surgery_Schwartz

Surgery_Schwartz. parasitic losses, sequestration, or third-space edema because the lost volume no longer participates in the normal functions of the ECF.Until the 1960s saline solutions were withheld during sur-gery. Administered saline was retained and was felt to be an inappropriate challenge to a physiologic response of intraopera-tive salt intolerance. Basic and clinical research began to change this concept,33,34 eventually leading to the current concept that saline administration is necessary to restore the obligate ECF losses noted earlier. Although no accurate formula can predict intraoperative fluid needs, replacement of ECF during surgery often requires 500 to 1000 mL/h of a balanced salt solution to support homeostasis. The addition of albumin or other colloidcontaining solutions to intraoperative fluid therapy is not neces-sary. Manipulation of colloid oncotic forces by albumin infusion during major vascular surgery showed no advantage in support-ing cardiac function or avoiding the


Surgery_Schwartz

Surgery_Schwartz. fluid therapy is not neces-sary. Manipulation of colloid oncotic forces by albumin infusion during major vascular surgery showed no advantage in support-ing cardiac function or avoiding the accumulation of extravas-cular lung water.35Postoperative Fluid TherapyPostoperative fluid therapy should be based on the patient’s current estimated volume status and projected ongoing fluid losses. Any deficits from either preoperative or intraoperative losses should be corrected, and ongoing requirements should be included along with maintenance fluids. Third-space losses, although difficult to measure, should be included in fluid replacement strategies. In the initial postoperative period, an isotonic solution should be administered. The adequacy of resuscitation should be guided by the restoration of acceptable values for vital signs and urine output and, in more complicated cases, by the correction of base deficit or lactate. Adjuncts to assessing volume status in the postoperative patient


Surgery_Schwartz

Surgery_Schwartz. of acceptable values for vital signs and urine output and, in more complicated cases, by the correction of base deficit or lactate. Adjuncts to assessing volume status in the postoperative patient include such tools as a straight leg raise, point-of-care ultrasound, and assessment of respiratory variation via use of an arterial cath-eter in a mechanically ventilated patient. After the initial 24 to 48 hours, fluids can be changed to 5% dextrose in 0.45% saline in patients unable to tolerate enteral nutrition. If normal renal function and adequate urine output are present, potassium may be added to the IV fluids. Daily fluid orders should begin with assessment of the patient’s volume status and assessment of electrolyte abnormalities. There is rarely a need to check elec-trolyte levels in the first few days of an uncomplicated post-operative course. However, postoperative diuresis may require attention to replacement of urinary potassium loss. All measured losses, including losses