3

chapter Fluid and Electrolyte Management

of the Surgical Patient
G. Tom Shires III

Introduction 65 Volume Control / 68 Postoperative Fluid Therapy / 80

Body Fluids 65 Concentration Changes / 69 Special Considerations for the
Total Body Water / 65 Composition Changes: Etiology and Postoperative Patient / 80
Fluid Compartments / 65 Diagnosis / 70 Electrolyte Abnormalities in
Composition of Fluid Acid-Base Balance / 73 Specific Surgical Patients 80
Compartments / 65 Fluid and Electrolyte Therapy 76 Neurologic Patients / 80
Osmotic Pressure / 66 Parenteral Solutions / 76 Malnourished Patients: Refeeding
Alternative Resuscitative Fluids / 76 Syndrome / 81
Body Fluid Changes 67
Correction of Life-Threatening Acute Renal Failure Patients / 81
Normal Exchange of Fluid and
Electrolytes / 67 Electrolyte Abnormalities / 77 Cancer Patients / 81
Classification of Body Fluid Changes / 67 Preoperative Fluid Therapy / 78
Disturbances in Fluid Balance / 68 Intraoperative Fluid Therapy / 80

INTRODUCTION of their total body weight comprised of water. This decreases

to approximately 65% by 1 year of age and thereafter remains
Fluid and electrolyte management is paramount to the care of fairly constant.
the surgical patient. Changes in both fluid volume and electro-
lyte composition occur preoperatively, intraoperatively, and
Fluid Compartments
postoperatively, as well as in response to trauma and sepsis. The
TBW is divided into three functional fluid compartments:
sections that follow review the normal anatomy of body fluids,
plasma, extravascular interstitial fluid, and intracellular fluid
electrolyte composition and concentration abnormalities and
(Fig. 3-1). The extracellular fluids (ECF), plasma and intersti-
1 treatments, common metabolic derangements, and alterna-
tive resuscitative fluids. These concepts are then discussed
tial fluid, together compose about one third of the TBW, and the
intracellular compartment composes the remaining two thirds.
in relationship to management of specific surgical patients and
The extracellular water composes 20% of the total body weight
their commonly encountered fluid and electrolyte abnormalities.
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,
BODY FLUIDS
with the largest proportion in the skeletal muscle mass. ECF
Total Body Water is measured using indicator dilution methods. The distribution
Water constitutes approximately 50% to 60% of total body volumes of NaBr and radioactive sulfate have been used to mea-
weight. The relationship between total body weight and total sure ECF in clinical research. Measurement of the intracellular
body water (TBW) is relatively constant for an individual and compartment is then determined indirectly by subtracting the
is primarily a reflection of body fat. Lean tissues such as muscle measured ECF from the simultaneous TBW measurement.
and solid organs have higher water content than fat and bone.
As a result, young, lean males have a higher proportion of body Composition of Fluid Compartments 
weight as water than elderly or obese individuals. Deuterium The normal chemical composition of the body fluid compart-
oxide and tritiated water have been used in clinical research ments is shown in Fig. 3-2. The ECF compartment is bal-
to measure TBW by indicator dilution methods. In an average 2 anced between sodium, the principal cation, and chloride
young adult male, TBW accounts for 60% of total body weight, and bicarbonate, the principal anions. The intracellular fluid
whereas in an average young adult female, it is 50%.1 The lower compartment is composed primarily of the cations potassium
percentage of TBW in females correlates with a higher percent- and magnesium, and the anions phosphate and sulfate, and
age of adipose tissue and lower percentage of muscle mass proteins. The concentration gradient between compartments is
in most. Estimates of percentage of TBW should be adjusted maintained by adenosine triphosphate–driven sodium-potassium
downward approximately 10% to 20% for obese individuals and pumps located with in the cell membranes. The composition of
upward by 10% for malnourished individuals. The highest per- the plasma and interstitial fluid differs only slightly in ionic
centage of TBW is found in newborns, with approximately 80% composition. The slightly higher protein content (organic anions)

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 Key Points
1 Proper management of fluid and electrolytes facilitates crucial 5 Although active investigation continues, alternative resus-
homeostasis that allows cardiovascular perfusion, organ system citation fluids have limited clinical utility, other than the
function, and cellular mechanisms to respond to surgical illness. correction of specific electrolyte abnormalities.
2 Knowledge of the compartmentalization of body fluids forms the 6 Most acute surgical illnesses are accompanied by some
basis for understanding pathologic shifts in these fluid spaces in degree of volume loss or redistribution. Consequently, iso-
disease states. Although difficult to quantify, a deficiency in the tonic fluid administration is the most common initial intra-
functional extracellular fluid compartment often requires resus- venous fluid strategy, while attention is being given to
citation with isotonic fluids in surgical and trauma patients. alterations in concentration and composition.
3 Alterations in the concentration of serum sodium have pro- 7 Some surgical patients with neurologic illness, malnutri-
found effects on cellular function due to water shifts tion, acute renal failure, or cancer require special attention
between the intracellular and extracellular spaces. to well-defined, disease-specific abnormalities in fluid and
4 Different rates of compensation between respiratory and meta- electrolyte status.
bolic components of acid-base homeostasis require frequent
laboratory reassessment during therapy.

in plasma results in a higher plasma cation composition relative (milliequivalents per liter, or mEq/L), and the number of osmot-
to the interstitial fluid, as explained by the Gibbs-Donnan equi- ically active ions per unit volume (milliosmoles per liter, or
librium equation. Proteins add to the osmolality of the plasma mOsm/L). The concentration of electrolytes usually is expressed
and contribute to the balance of forces that determine fluid bal- in terms of the chemical combining activity, or equivalents. An
ance across the capillary endothelium. Although the movement equivalent of an ion is its atomic weight expressed in grams
of ions and proteins between the various fluid compartments is divided by the valence:
restricted, water is freely diffusible. Water is distributed evenly
throughout all fluid compartments of the body so that a given Equivalent = atomic weight (g)/valence
volume of water increases the volume of any one compartment
relatively little. Sodium, however, is confined to the ECF com- For univalent ions such as sodium, 1 mEq is the same as
partment, and because of its osmotic and electrical properties, 1 mmol. For divalent ions such as magnesium, 1 mmol equals
it remains associated with water. Therefore, sodium-containing 2 mEq. The number of milliequivalents of cations must be bal-
fluids are distributed throughout the ECF and add to the vol- anced by the same number of milliequivalents of anions. How-
ume of both the intravascular and interstitial spaces. Although ever, the expression of molar equivalents alone does not allow a
the administration of sodium-containing fluids expands the physiologic comparison of solutes in a solution.
intravascular volume, it also expands the interstitial space by The movement of water across a cell membrane depends
approximately three times as much as the plasma. primarily on osmosis. To achieve osmotic equilibrium, water
moves across a semipermeable membrane to equalize the
Osmotic Pressure concentration on both sides. This movement is determined by
The physiologic activity of electrolytes in solution depends the concentration of the solutes on each side of the membrane.
on the number of particles per unit volume (millimoles per Osmotic pressure is measured in units of osmoles (osm) or mil-
liter, or mmol/L), the number of electric charges per unit volume liosmoles (mOsm) that refer to the actual number of osmotically

% of Total body weight Volume of TBW Male (70 kg) Female (60 kg)

Plasma 5% Extracellular volume 14,000 mL 10,000 mL

Interstitial Plasma 3500 mL 2500 mL

fluid 15%
Interstitial 10,500 mL 7500 mL

Intracellular volume 28,000 mL 20,000 mL

Intracellular
volume 40%
42,000 mL 30,000 mL

Figure 3-1. Functional body fluid

compartments. TBW = total body
66 water.

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 200 mEq/L 200 mEq/L 67
CATIONS ANIONS

CHAPTER 3
154 mEq/L 154 mEq/L 153 mEq/L 153 mEq/L K+ 150 HPO43–
150
CATIONS ANIONS CATIONS ANIONS SO 42–

Na+ 142 CI− 103 Na+ 144 CI− 114

Fluid and Electrolyte Management of the Surgical Patient

HCO3 − 27

SO4 2– HCO3− 30 HCO3− 10

3
PO43–
SO42–
K+ 4 3
PO43–
K+ 4
Mg2+ 40 Protein 40
Organic
Acids 5 Organic
Ca2+ 5 Ca2+ 3
Acids 5

Mg2+ 3 Protein 16 Mg2+ 2 Protein 1 Na+ 10

Plasma Interstitial Intracellular Figure 3-2.  Chemical composition of

fluid fluid body fluid compartments.

active particles. For example, 1 mmol of sodium chloride con- extracted from solid foods. Daily water losses include 800 to
tributes to 2 mOsm (one from sodium and one from chloride). 1200 mL in urine, 250 mL in stool, and 600 mL in insensible
The principal determinants of osmolality are the concentrations of losses. Insensible losses of water occur through both the skin
sodium, glucose, and urea (blood urea nitrogen, or BUN): (75%) and lungs (25%) and can be increased by such factors as
fever, hypermetabolism, and hyperventilation. Sensible water
Calculated serum osmolality = 2 sodium + losses such as sweating or pathologic loss of gastrointestinal
(glucose/18) + (BUN/2.8) (GI) fluids vary widely, but these include the loss of electrolytes
as well as water (Table 3-1). To clear the products of metabo-
The osmolality of the intracellular and extracellular fluids
lism, the kidneys must excrete a minimum of 500 to 800 mL of
is maintained between 290 and 310 mOsm in each compartment.
urine per day, regardless of the amount of oral intake.
Because cell membranes are permeable to water, any change in
The typical individual consumes 3 to 5 g of dietary salt per
osmotic pressure in one compartment is accompanied by a redis-
day, with the balance maintained by the kidneys. With hypo-
tribution of water until the effective osmotic pressure between
natremia or hypovolemia, sodium excretion can be reduced to
compartments is equal. For example, if the ECF concentration
as little as 1 mEq/d or maximized to as much as 5000 mEq/d
of sodium increases, there will be a net movement of water from
to achieve balance except in people with salt-wasting kidneys.
the intracellular to the extracellular compartment. Conversely,
Sweat is hypotonic, and sweating usually results in only a small
if the ECF concentration of sodium decreases, water will move
sodium loss. GI losses are isotonic to slightly hypotonic and
into the cells. Although the intracellular fluid shares in losses
contribute little to net gain or loss of free water when measured
that involve a change in concentration or composition of the
and appropriately replaced by isotonic salt solutions.
ECF, an isotonic change in volume in either one of the com-
partments is not accompanied by the net movement of water as Classification of Body Fluid Changes
long as the ionic concentration remains the same. For practical Disorders in fluid balance may be classified into three general
clinical purposes, most significant gains and losses of body fluid categories: disturbances in (a) volume, (b) concentration, and
are directly from the extracellular compartment. (c) composition. Although each of these may occur simultane-
ously, each is a separate entity with unique mechanisms demand-
BODY FLUID CHANGES ing individual correction. Isotonic gain or loss of salt solution
results in extracellular volume changes, with little impact on
Normal Exchange of Fluid and Electrolytes intracellular fluid volume. If free water is added or lost from the
The healthy person consumes an average of 2000 mL of water ECF, water will pass between the ECF and intracellular fluid
per day, approximately 75% from oral intake and the rest until solute concentration or osmolarity is equalized between

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 68 Table 3-1
Water exchange (60- to 80-kg man)

Average Daily
PART I

Routes Volume (mL) Minimal (mL) Maximal (mL)

H2O gain:
 Sensible:
  Oral fluids 800–1500 0 1500/h
BASIC CONSIDERATIONS

  Solid foods 500–700 0 1500

 Insensible:
   Water of oxidation 250 125 800
   Water of solution 0 0 500
H2O loss:
 Sensible:
  Urine 800–1500 300 1400/h
  Intestinal 0–250 0 2500/h
  Sweat 0 0 4000/h
 Insensible:
   Lungs and skin 600 600 1500

the compartments. Unlike with sodium, the concentration of heart failure and pulmonary edema in response to only a moder-
most other ions in the ECF can be altered without significant ate volume excess.
change in the total number of osmotically active particles, pro-
ducing only a compositional change. For instance, doubling the Volume Control
serum potassium concentration will profoundly alter myocardial Volume changes are sensed by both osmoreceptors and baro-
function without significantly altering volume or concentration receptors. Osmoreceptors are specialized sensors that detect
of the fluid spaces. even small changes in fluid osmolality and drive changes in
thirst and diuresis through the kidneys.2 For example, when
Disturbances in Fluid Balance plasma osmolality is increased, thirst is stimulated and water
Extracellular volume deficit is the most common fluid disorder consumption increases, although the exact cell mechanism is not
in surgical patients and can be either acute or chronic. Acute known.3 Additionally, the hypothalamus is stimulated to secrete
volume deficit is associated with cardiovascular and central ner- vasopressin, which increases water reabsorption in the kidneys.
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 blood urea
Table 3-2
nitrogen level if the deficit is severe enough to reduce glomeru-
lar filtration and hemoconcentration. Urine osmolality usually Signs and symptoms of volume disturbances
will be higher than serum osmolality, and urine sodium will be
low, typically <20 mEq/L. Serum sodium concentration does System Volume Deficit Volume Excess
not necessarily reflect volume status and therefore may be high, Generalized Weight loss Weight gain
normal, or low when a volume deficit is present. The most com-
Decreased skin turgor Peripheral edema
mon cause of volume deficit in surgical patients is a loss of GI
fluids (Table 3-3) from nasogastric suction, vomiting, diarrhea, Cardiac Tachycardia Increased cardiac
or enterocutaneous fistula. In addition, sequestration secondary output
to soft tissue injuries, burns, and intra-abdominal processes such Orthostasis/ Increased central
as peritonitis, obstruction, or prolonged surgery can also lead to hypotension venous pressure
massive volume deficits. Collapsed neck veins Distended neck veins
Extracellular volume excess may be iatrogenic or second-
Murmur
ary to renal dysfunction, congestive heart failure, or cirrhosis.
Both plasma and interstitial volumes usually are increased. Renal Oliguria —
Symptoms are primarily pulmonary and cardiovascular (see Azotemia
Table 3-2). In fit patients, edema and hyperdynamic circula- GI Ileus Bowel edema
tion are common and well tolerated. However, the elderly and
Pulmonary — Pulmonary edema
patients with cardiac disease may quickly develop congestive

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Table 3-3 69

Composition of GI secretions

CHAPTER 3
Type of Secretion Volume (mL/24 h) Na (mEq/L) K (mEq/L) Cl (mEq/L) HCO3− (mEq/L)
Stomach 1000–2000 60–90 10–30 100–130 0
Small intestine 2000–3000 120–140 5–10 90–120 30–40
Colon — 60 30 40 0
Pancreas 600–800 135–145 5–10 70–90 95–115

Fluid and Electrolyte Management of the Surgical Patient

Bile 300–800 135–145 5–10 90–110 30–40

Together, these two mechanisms return the plasma osmolality intracellular to the extracellular space. Hyponatremia therefore
to normal. Baroreceptors also modulate volume in response to can be seen when the effective osmotic pressure of the extracel-
changes in pressure and circulating volume through specialized lular compartment is normal or even high. When hyponatremia
pressure sensors located in the aortic arch and carotid sinuses.4 in the presence of hyperglycemia is being evaluated, the cor-
Baroreceptor responses are both neural, through sympathetic and rected sodium concentration should be calculated as follows:
parasympathetic pathways, and hormonal, through substances
including renin-angiotensin, aldosterone, atrial natriuretic pep- For every 100-mg/dL increment in plasma glucose above
tide, and renal prostaglandins. The net result of alterations in normal, the plasma sodium should
renal sodium excretion and free water reabsorption is restoration decrease by 1.6 mEq/L
of volume to the normal state.
Lastly, extreme elevations in plasma lipids and proteins can
Concentration Changes cause pseudohyponatremia, because there is no true decrease in
Changes in serum sodium concentration are inversely pro- extracellular sodium relative to water.
portional to TBW. Therefore, abnormalities in TBW are Signs and symptoms of hyponatremia (Table 3-4) are
3 reflected by abnormalities in serum sodium levels. dependent on the degree of hyponatremia and the rapidity with
Hyponatremia.  A low serum sodium level occurs when there which it occurred. Clinical manifestations primarily have a
is an excess of extracellular water relative to sodium. Extracel- central nervous system origin and are related to cellular water
lular volume can be high, normal, or low (Fig. 3-3). In most intoxication and associated increases in intracranial pressure.
cases of hyponatremia, sodium concentration is decreased as a Oliguric renal failure also can be a rapid complication in the
consequence of either sodium depletion or dilution.5 Dilutional setting of severe hyponatremia.
hyponatremia frequently results from excess extracellular water A systematic review of the etiology of hyponatremia
and therefore is associated with a high extracellular volume sta- should reveal its cause in a given instance. Hyperosmolar
tus. Excessive oral water intake or iatrogenic intravenous (IV) causes, including hyperglycemia or mannitol infusion and pseu-
excess free water administration can cause hyponatremia. Post- dohyponatremia, should be easily excluded. Next, depletional
operative patients are particularly prone to increased secretion versus dilutional causes of hyponatremia are evaluated. In the
of antidiuretic hormone (ADH), which increases reabsorption absence of renal disease, depletion is associated with low urine
of free water from the kidneys with subsequent volume expan- sodium levels (<20 mEq/L), whereas renal sodium wasting
sion and hyponatremia. This is usually self-limiting in that both shows high urine sodium levels (>20 mEq/L). Dilutional causes
hyponatremia and volume expansion decrease ADH secretion. of hyponatremia usually are associated with hypervolemic cir-
Additionally, a number of drugs can cause water retention and culation. A normal volume status in the setting of hyponatremia
subsequent hyponatremia, such as the antipsychotics and tricy- should prompt an evaluation for a syndrome of inappropriate
clic antidepressants as well as angiotensin-converting enzyme secretion of ADH.
inhibitors. The elderly are particularly susceptible to drug- Hypernatremia.  Hypernatremia results from either a loss of
induced hyponatremia. Physical signs of volume overload usu- free water or a gain of sodium in excess of water. Like hypo-
ally are absent, and laboratory evaluation reveals hemodilution. natremia, it can be associated with an increased, normal, or
Depletional causes of hyponatremia are associated with either a decreased extracellular volume (see Fig. 3-3). Hypervolemic
decreased intake or increased loss of sodium-containing fluids. hypernatremia usually is caused either by iatrogenic adminis-
A concomitant ECF volume deficit is common. Causes include tration of sodium-containing fluids, including sodium bicarbon-
decreased sodium intake, such as consumption of a low-sodium ate, or mineralocorticoid excess as seen in hyperaldosteronism,
diet or use of enteral feeds, which are typically low in sodium; Cushing’s syndrome, and congenital adrenal hyperplasia. Urine
GI losses from vomiting, prolonged nasogastric suctioning, or sodium concentration is typically >20 mEq/L, and urine osmo-
diarrhea; and renal losses due to diuretic use or primary renal larity is >300 mOsm/L. Normovolemic hypernatremia can
disease. result from renal causes, including diabetes insipidus, diuretic
Hyponatremia also can be seen with an excess of solute use, and renal disease, or from nonrenal water loss from the
relative to free water, such as with untreated hyperglycemia or GI tract or skin, although the same conditions can result in
mannitol administration. Glucose exerts an osmotic force in the hypovolemic hypernatremia. When hypovolemia is present, the
extracellular compartment, causing a shift of water from the urine sodium concentration is <20 mEq/L and urine osmolarity

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 70
Hyponatremia

Volume status
PART I

High Normal Low

Increased intake Hyperglycemia Decreased sodium intake

BASIC CONSIDERATIONS

Postoperative ADH secretion ↑ Plasma Iipids/proteins GI losses

Drugs SIADH Renal losses

Water intoxication Diuretics

Diuretics Primary renal disease

Hypernatremia

Volume status

High Normal Low

Iatrogenic sodium administration Nonrenal water loss Nonrenal water loss

Mineralocorticoid excess Skin Skin

Aldosteronism GI GI

Cushing’s disease Renal water loss Renal water loss

Congenital adrenal hyperplasia Renal disease Renal (tubular) disease

Diuretics Osmotic diuretics

Figure 3-3. Evaluation of sodium
abnormalities. ADH = antidiuretic
Diabetes insipidus Diabetes insipidus
hormone; SIADH = syndrome of
inappropriate secretion of antidi-
Adrenal failure
uretic hormone.

is <300 to 400 mOsm/L. Nonrenal water loss can occur second- can range from restlessness and irritability to seizures, coma,
ary to relatively isotonic GI fluid losses such as that caused by and death. The classic signs of hypovolemic hypernatremia,
diarrhea, to hypotonic skin fluid losses such as loss due to fever, (tachycardia, orthostasis, and hypotension) may be present, as
or to losses via tracheotomies during hyperventilation. Addi- well as the unique findings of dry, sticky mucous membranes.
tionally, thyrotoxicosis can cause water loss, as can the use of
hypertonic glucose solutions for peritoneal dialysis. With non- Composition Changes: Etiology and Diagnosis
renal water loss, the urine sodium concentration is <15 mEq/L Potassium Abnormalities.  The average dietary intake of
and the urine osmolarity is >400 mOsm/L. potassium is approximately 50 to 100 mEq/d, which in the
Symptomatic hypernatremia usually occurs only in patients absence of hypokalemia is excreted primarily in the urine.
with impaired thirst or restricted access to fluid, because thirst Extracellular potassium is maintained within a narrow range,
will result in increased water intake. Symptoms are rare until principally by renal excretion of potassium, which can range
the serum sodium concentration exceeds 160 mEq/L but, once from 10 to 700 mEq/d. Although only 2% of the total body
present, are associated with significant morbidity and mortality. potassium (4.5 mEq/L × 14 L = 63 mEq) is located within the
Because symptoms are related to hyperosmolarity, central ner- extracellular compartment, this small amount is critical to car-
vous system effects predominate (see Table 3-4). Water shifts diac and neuromuscular function; thus, even minor changes
from the intracellular to the extracellular space in response to a can have major effects on cardiac activity. The intracellular
hyperosmolar extracellular space, which results in cellular dehy- and extracellular distribution of potassium is influenced by a
dration. This can put traction on the cerebral vessels and lead to number of factors, including surgical stress, injury, acidosis,
subarachnoid hemorrhage. Central nervous system symptoms and tissue catabolism.

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Table 3-4 Table 3-5 71

Clinical manifestations of abnormalities in serum Etiology of potassium abnormalities

sodium level Hyperkalemia

CHAPTER 3
Increased intake
Body System Hyponatremia   Potassium supplementation
Central nervous Headache, confusion, hyperactive or   Blood transfusions
system hypoactive deep tendon reflexes, seizures,  Endogenous load/destruction: hemolysis, rhabdomyolysis,
coma, increased intracranial pressure crush injury, gastrointestinal hemorrhage
Increased release

Fluid and Electrolyte Management of the Surgical Patient

Musculoskeletal Weakness, fatigue, muscle cramps/
twitching  Acidosis
 Rapid rise of extracellular osmolality (hyperglycemia or
GI Anorexia, nausea, vomiting, watery mannitol)
diarrhea Impaired excretion
Cardiovascular Hypertension and bradycardia   Potassium-sparing diuretics
if intracranial pressure increases   Renal insufficiency/failure
significantly
Hypokalemia
Tissue Lacrimation, salivation
Inadequate intake
Renal Oliguria  Dietary, potassium-free intravenous fluids, potassium-
Body System Hypernatremia deficient TPN
Central nervous Restlessness, lethargy, ataxia, irritability, Excessive potassium excretion
system tonic spasms, delirium, seizures, coma  Hyperaldosteronism
 Medications
Musculoskeletal Weakness GI losses
Cardiovascular Tachycardia, hypotension, syncope   Direct loss of potassium from GI fluid (diarrhea)
Tissue Dry sticky mucous membranes, red  Renal loss of potassium (to conserve sodium in response
swollen tongue, decreased saliva and tears to gastric losses)
Renal Oliguria
Metabolic Fever
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
Hyperkalemia  Hyperkalemia is defined as a serum potassium P wave, prolonged PR interval (first-degree block), sine wave
concentration above the normal range of 3.5 to 5.0 mEq/L. formation, and ventricular fibrillation.
It is caused by excessive potassium intake, increased release
Hypokalemia Hypokalemia is much more common than
of potassium from cells, or impaired potassium excretion by
hyperkalemia in the surgical patient. It may be caused by inad-
the kidneys (Table 3-5).6 Increased intake can be either from
equate potassium intake; excessive renal potassium excretion;
oral or IV supplementation, or from red cell lysis after transfu-
potassium loss in pathologic GI secretions, such as with diar-
sion. Hemolysis, rhabdomyolysis, and crush injuries can dis-
rhea, fistulas, vomiting, or high nasogastric output; or intracel-
rupt cell membranes and release intracellular potassium into
lular shifts from metabolic alkalosis or insulin therapy (see
the ECF. Acidosis and a rapid rise in extracellular osmolality
Table 3-5). The change in potassium associated with alkalosis
from hyperglycemia or IV mannitol can raise serum potassium
can be calculated by the following formula:
levels by causing a shift of potassium ions to the extracellular
compartment.7 Because 98% of total body potassium is in the Potassium decreases by 0.3 mEq/L for
intracellular fluid compartment, even small shifts of intracel- every 0.1 increase in pH above normal.
lular potassium out of the intracellular fluid compartment can
lead to a significant rise in extracellular potassium. A number Additionally, drugs such as amphotericin, aminoglyco-
of medications can contribute to hyperkalemia, particularly in sides, cisplatin, and ifosfamide that induce magnesium depletion
the presence of renal insufficiency, including potassium-sparing cause renal potassium wastage.8,9 In cases in which potassium
diuretics, angiotensin-converting enzyme inhibitors, and non- deficiency is due to magnesium depletion,10 potassium repletion
steroidal anti-inflammatory drugs (NSAIDs). Spironolactone is difficult unless hypomagnesemia is first corrected.
and angiotensin-converting enzyme inhibitors interfere with The symptoms of hypokalemia (see Table 3-6), like those
aldosterone activity, inhibiting the normal renal mechanism of of hyperkalemia, are primarily related to failure of normal con-
potassium excretion. Acute and chronic renal insufficiency also tractility of GI smooth muscle, skeletal muscle, and cardiac mus-
impairs potassium excretion. cle. Findings may include ileus, constipation, weakness, fatigue,
Symptoms of hyperkalemia are primarily GI, neuromus- diminished tendon reflexes, paralysis, and cardiac arrest. In the
cular, and cardiovascular (Table 3-6). GI symptoms include setting of ECF depletion, symptoms may be masked initially
nausea, vomiting, intestinal colic, and diarrhea. Neuromuscu- and then worsened by further dilution during volume repletion.
lar symptoms range from weakness to ascending paralysis to ECG changes suggestive of hypokalemia include U waves,
respiratory failure. Early cardiovascular signs may be appar- T-wave flattening, ST-segment changes, and arrhythmias (with
ent from electrocardiogram (ECG) changes and eventually lead digitalis therapy).

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 72 Table 3-6
Clinical manifestations of abnormalities in potassium, magnesium, and calcium levels

Increased Serum Levels

PART I

System Potassium Magnesium Calcium

GI Nausea/vomiting, colic, diarrhea Nausea/vomiting Anorexia, nausea/vomiting,
abdominal pain
BASIC CONSIDERATIONS

Neuromuscular Weakness, paralysis, respiratory Weakness, lethargy, decreased Weakness, confusion, coma, bone
failure reflexes pain
Cardiovascular Arrhythmia, arrest Hypotension, arrest Hypertension, arrhythmia, polyuria
Renal — — Polydipsia
Decreased Serum Levels
System Potassium Magnesium Calcium
GI Ileus, constipation — —
Neuromuscular Decreased reflexes, fatigue, Hyperactive reflexes, muscle Hyperactive reflexes, paresthesias,
weakness, paralysis tremors, tetany, seizures carpopedal spasm, seizures
Cardiovascular Arrest Arrhythmia Heart failure

Calcium Abnormalities.  The vast majority of the body’s cal- Hypocalcemia  Hypocalcemia is defined as a serum calcium
cium is contained within the bone matrix, with <1% found in the level below 8.5 mEq/L or a decrease in the ionized calcium
ECF. Serum calcium is distributed among three forms: protein level below 4.2 mg/dL. The causes of hypocalcemia include
found (40%), complexed to phosphate and other anions (10%), pancreatitis, massive soft tissue infections such as necrotiz-
and ionized (50%). It is the ionized fraction that is responsible ing fasciitis, renal failure, pancreatic and small bowel fistulas,
for neuromuscular stability and can be measured directly. When hypoparathyroidism, toxic shock syndrome, abnormalities in
total serum calcium levels are measured, the albumin concentra- magnesium levels, and tumor lysis syndrome. In addition, tran-
tion must be taken into consideration: sient hypocalcemia commonly occurs after removal of a para-
thyroid adenoma due to atrophy of the remaining glands and
Adjust total serum calcium down by 0.8 mg/dL avid bone remineralization, and sometimes requires high-dose
for every 1 g/dL decrease in albumin. calcium supplementation.12 Additionally, malignancies asso-
ciated with increased osteoblastic activity, such as breast and
Unlike changes in albumin, changes in pH will affect the prostate cancer, can lead to hypocalcemia from increased bone
ionized calcium concentration. Acidosis decreases protein bind- formation.13 Calcium precipitation with organic anions is also a
ing, thereby increasing the ionized fraction of calcium. cause of hypocalcemia and may occur during hyperphosphate-
Daily calcium intake is 1 to 3 g/d. Most of this is excreted mia from tumor lysis syndrome or rhabdomyolysis. Pancreatitis
via the bowel, with urinary excretion relatively low. Total body may sequester calcium via chelation with free fatty acids. Mas-
calcium balance is under complex hormonal control, but distur- sive blood transfusion with citrate binding is another mecha-
bances in metabolism are relatively long term and less important nism.14,15 Hypocalcemia rarely results solely from decreased
in the acute surgical setting. However, attention to the critical role intake, because bone reabsorption can maintain normal levels
of ionized calcium in neuromuscular function often is required. for prolonged periods.
Hypercalcemia  Hypercalcemia is defined as a serum calcium Asymptomatic hypocalcemia may occur when hypopro-
level above the normal range of 8.5 to 10.5 mEq/L or an increase teinemia results in a normal ionized calcium level. Conversely,
in the ionized calcium level above 4.2 to 4.8 mg/dL. Primary symptoms can develop with a normal serum calcium level
hyperparathyroidism in the outpatient setting and malignancy during alkalosis, which decreases ionized calcium. In general,
in hospitalized patients, from either bony metastasis or secre- neuromuscular and cardiac symptoms do not occur until the ion-
tion of parathyroid hormone–related protein, account for most ized fraction falls below 2.5 mg/dL (see Table 3-6). Clinical
cases of symptomatic hypercalcemia.11 Symptoms of hypercal- findings may include paresthesias of the face and extremities,
cemia (see Table 3-6), which vary with the degree of severity, muscle cramps, carpopedal spasm, stridor, tetany, and seizures.
include neurologic impairment, musculoskeletal weakness and Patients will demonstrate hyperreflexia and may exhibit positive
pain, renal dysfunction, and GI symptoms of nausea, vomiting, Chvostek’s sign (spasm resulting from tapping over the facial
and abdominal pain. Cardiac symptoms can be manifest as nerve) and Trousseau’s sign (spasm resulting from pressure
hypertension, cardiac arrhythmias, and a worsening of digitalis applied to the nerves and vessels of the upper extremity with
toxicity. ECG changes in hypercalcemia include shortened QT a blood pressure cuff). Hypocalcemia may lead to decreased
interval, prolonged PR and QRS intervals, increased QRS volt- cardiac contractility and heart failure. ECG changes of hypocal-
age, T-wave flattening and widening, and atrioventricular block cemia include prolonged QT interval, T-wave inversion, heart
(which can progress to complete heart block and cardiac arrest). block, and ventricular fibrillation.

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Phosphorus Abnormalities.  Phosphorus is the primary intra- Hypomagnesemia  Magnesium depletion is a common prob- 73
cellular divalent anion and is abundant in metabolically active lem in hospitalized patients, particularly in the critically ill.16
cells. Phosphorus is involved in energy production during gly- The kidney is primarily responsible for magnesium homeosta-
colysis and is found in high-energy phosphate products such sis through regulation by calcium/magnesium receptors on the

CHAPTER 3
as adenosine triphosphate. Serum phosphate levels are tightly renal tubular cells that respond to serum magnesium concentra-
controlled by renal excretion. tions.17 Hypomagnesemia may result from alterations of intake,
renal excretion, and pathologic losses. Poor intake may occur in
Hyperphosphatemia  Hyperphosphatemia can be due to
cases of starvation, alcoholism, prolonged IV fluid therapy, and
decreased urinary excretion, increased intake, or endogenous
TPN with inadequate supplementation of magnesium. Losses are
mobilization of phosphorus. Most cases of hyperphosphatemia
seen in cases of increased renal excretion from alcohol abuse,

Fluid and Electrolyte Management of the Surgical Patient

are seen in patients with impaired renal function. Hypoparathy-
diuretic use, administration of amphotericin B, and primary aldo-
roidism or hyperthyroidism also can decrease urinary excretion
steronism, as well as GI losses from diarrhea, malabsorption,
of phosphorus and thus lead to hyperphosphatemia. Increased
and acute pancreatitis. The magnesium ion is essential for proper
release of endogenous phosphorus can be seen in association with
function of many enzyme systems. Depletion is characterized by
any clinical condition that results in cell destruction, including
neuromuscular and central nervous system hyperactivity. Symp-
rhabdomyolysis, tumor lysis syndrome, hemolysis, sepsis, severe
toms are similar to those of calcium deficiency, including hyper-
hypothermia, and malignant hyperthermia. Excessive phosphate
active reflexes, muscle tremors, tetany, and positive Chvostek’s
administration from IV hyperalimentation solutions or phosphorus-
and Trousseau’s signs (see Table 3-6). Severe deficiencies can
containing laxatives may also lead to elevated phosphate levels.
lead to delirium and seizures. A number of ECG changes also
Most cases of hyperphosphatemia are asymptomatic, but signifi-
can occur and include prolonged QT and PR intervals, ST-seg-
cant prolonged hyperphosphatemia can lead to metastatic deposi-
ment depression, flattening or inversion of P waves, torsades
tion of soft tissue calcium-phosphorus complexes.
de pointes, and arrhythmias. Hypomagnesemia is important
Hypophosphatemia Hypophosphatemia can be due to a not only because of its direct effects on the nervous system but
decrease in phosphorus intake, an intracellular shift of phospho- also because it can produce hypocalcemia and lead to persis-
rus, or an increase in phosphorus excretion. Decreased GI uptake tent hypokalemia. When hypokalemia or hypocalcemia coex-
due to malabsorption or administration of phosphate binders and ists with hypomagnesemia, magnesium should be aggressively
decreased dietary intake from malnutrition are causes of chronic replaced to assist in restoring potassium or calcium homeostasis.
hypophosphatemia. Most acute cases are due to an intracellular
Acid-Base Balance
shift of phosphorus in association with respiratory alkalosis,
insulin therapy, refeeding syndrome, and hungry bone syn- Acid-Base Homeostasis.  The pH of body fluids is maintained
drome. Clinical manifestations of hypophosphatemia usually within a narrow range despite the ability of the kidneys to gen-
are absent until levels fall significantly. In general, symptoms erate large amounts of HCO3− and the normal large acid load
are related to adverse effects on the oxygen availability of tissue produced as a by-product of metabolism. This endogenous acid
and to a decrease in high-energy phosphates, and can be mani- load is efficiently neutralized by buffer systems and ultimately
fested as cardiac dysfunction or muscle weakness. excreted by the lungs and kidneys.
Important buffers include intracellular proteins and phos-
Magnesium Abnormalities.  Magnesium is the fourth most phates and the extracellular bicarbonate–carbonic acid system.
common mineral in the body and, like potassium, is found pri- Compensation for acid-base derangements can be by respiratory
marily in the intracellular compartments. Approximately one mechanisms (for metabolic derangements) or metabolic mecha-
half of the total body content of 2000 mEq is incorporated in nisms (for respiratory derangements). Changes in ventilation in
bone and is slowly exchangeable. Of the fraction found in the response to metabolic abnormalities are mediated by hydrogen-
extracellular space, one third is bound to serum albumin. There- sensitive chemoreceptors found in the carotid body and brain
fore, the plasma level of magnesium may be a poor indicator stem. Acidosis stimulates the chemoreceptors to increase ven-
of total body stores in the presence of hypoalbuminemia. Mag- tilation, whereas alkalosis decreases the activity of the chemo-
nesium should be replaced until levels are in the upper limit of receptors and thus decreases ventilation. The kidneys provide
normal. The normal dietary intake is approximately 20 mEq/d compensation for respiratory abnormalities by either increasing
and is excreted in both the feces and urine. The kidneys have a or decreasing bicarbonate reabsorption in response to respiratory
remarkable ability to conserve magnesium, with renal excretion acidosis or alkalosis, respectively. Unlike the prompt change in
<1 mEq/d during magnesium deficiency. ventilation that occurs with metabolic abnormalities, the com-
Hypermagnesemia  Hypermagnesemia is rare but can be seen pensatory response in the kidneys to respiratory abnormalities
with severe renal insufficiency and parallel changes in potas- is delayed. Significant compensation may not begin for 6 hours
sium excretion. Magnesium-containing antacids and laxatives and then may continue for several days. Because of this delayed
can produce toxic levels in patients with renal failure. Excess compensatory response, respiratory acid-base derangements
intake in conjunction with total parenteral nutrition (TPN), or before renal compensation are classified as acute, whereas those
rarely massive trauma, thermal injury, and severe acidosis, persisting after renal compensation are categorized as chronic.
may be associated with symptomatic hypermagnesemia. Clini- 4 The predicted compensatory changes in response to meta-
bolic or respiratory derangements are listed in Table 3-7.18
cal examination (see Table 3-6) may find nausea and vomit-
ing; neuromuscular dysfunction with weakness, lethargy, and If the predicted change in pH is exceeded, then a mixed acid-
hyporeflexia; and impaired cardiac conduction leading to hypo- base abnormality may be present (Table 3-8).
tension and arrest. ECG changes are similar to those seen with Metabolic Derangements 
hyperkalemia and include increased PR interval, widened QRS Metabolic Acidosis  Metabolic acidosis results from an
complex, and elevated T waves. increased intake of acids, an increased generation of acids, or an

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 74 Table 3-7
• β-Hydroxybutyrate and acetoacetate in ketoacidosis
• Lactate in lactic acidosis
Predicted changes in acid-base disorders
• Organic acids in renal insufficiency
Disorder Predicted Change A common cause of severe metabolic acidosis in surgi-
PART I

Metabolic cal patients is lactic acidosis. In circulatory shock, lactate is

  Metabolic acidosis Pco2 = 1.5 × HCO3− + 8 produced in the presence of hypoxia from inadequate tissue
  Metabolic alkalosis Pco2 = 0.7 × HCO3− + 21 perfusion. The treatment is to restore perfusion with volume
resuscitation rather than to attempt to correct the abnormality
Respiratory with exogenous bicarbonate. With adequate perfusion, the lactic
BASIC CONSIDERATIONS

  Acute respiratory acidosis Δ pH = (Pco2 – 40) × 0.008 acid is rapidly metabolized by the liver and the pH level returns
 Chronic respiratory Δ pH = (Pco2 – 40) × 0.003 to normal. In clinical studies of lactic acidosis and ketoacido-
 acidosis sis, the administration of bicarbonate has not reduced morbidity
  Acute respiratory alkalosis Δ pH = (40 – Pco2) × 0.008 or mortality or improved cellular function.20 The overzealous
 Chronic respiratory Δ pH = (40 – Pco2) × 0.017 administration of bicarbonate can lead to metabolic alkalosis,
 alkalosis which shifts the oxyhemoglobin dissociation curve to the left;
Pco2 = partial pressure of carbon dioxide. this interferes with oxygen unloading at the tissue level and can
be associated with arrhythmias that are difficult to treat. An
additional disadvantage is that sodium bicarbonate actually can
exacerbate intracellular acidosis. Administered bicarbonate can
increased loss of bicarbonate (Table 3-9). The body responds by combine with the excess hydrogen ions to form carbonic acid;
several mechanisms, including producing buffers (extracellular this is then converted to CO2 and water, which thus raises the
bicarbonate and intracellular buffers from bone and muscle), partial pressure of CO2 (Pco2). This hypercarbia could com-
increasing ventilation (Kussmaul’s respirations), and increas- pound ventilation abnormalities in patients with underlying
ing renal reabsorption and generation of bicarbonate. The kid- acute respiratory distress syndrome. This CO2 can diffuse into
ney also will increase secretion of hydrogen and thus increase cells, but bicarbonate remains extracellular, which thus worsens
urinary excretion of NH4+ (H+ + NH3+ = NH4+). Evaluation of intracellular acidosis. Clinically, lactate levels may not be useful
a patient with a low serum bicarbonate level and metabolic aci- in directing resuscitation, although lactate levels may be higher
dosis includes determination of the anion gap (AG), an index in nonsurvivors of serious injury.21
of unmeasured anions. Metabolic acidosis with a normal AG results from exog-
enous acid administration (HCl or NH4+), from loss of bicar-
AG = (Na) – (Cl + HCO3) bonate due to GI disorders such as diarrhea and fistulas or
ureterosigmoidostomy, or from renal losses. In these settings,
The normal AG is <12 mmol/L and is due primarily to the the bicarbonate loss is accompanied by a gain of chloride;
albumin effect, so that the estimated AG must be adjusted for thus, the AG remains unchanged. To determine whether the
albumin (hypoalbuminemia reduces the AG).19 loss of bicarbonate has a renal cause, the urinary [NH4+] can
be measured. A low urinary [NH4+] in the face of hyperchlore-
Corrected AG = actual AG – [2.5(4.5 – albumin)]
mic acidosis would indicate that the kidney is the site of loss,
Metabolic acidosis with an increased AG occurs either and evaluation for renal tubular acidosis should be undertaken.
from ingestion of exogenous acid such as from ethylene gly- Proximal renal tubular acidosis results from decreased tubular
col, salicylates, or methanol, or from increased endogenous acid reabsorption of HCO3−, whereas distal renal tubular acidosis
production of the following: results from decreased acid excretion. The carbonic anhydrase

Table 3-8
Respiratory and metabolic components of acid-base disorders

Acute Uncompensated Chronic (Partially Compensated)

Plasma HCO3−a Plasma HCO3−a

Type of Acid-Base Pco2 (Respiratory (Metabolic Pco2 (Respiratory (Metabolic
Disorder pH Component) Component) pH Component) Component)
Respiratory acidosis ↓↓ ↑↑ N ↓ ↑↑ ↑
Respiratory alkalosis ↑↑ ↓↓ N ↑ ↓↓ ↓
Metabolic acidosis ↓↓ N ↓↓ ↓ ↓ ↓
Metabolic alkalosis ↑↑ N ↑↑ ↑ ↑? ↑
aMeasured as standard bicarbonate, whole blood buffer base, CO content, or CO combining power. The base excess value is positive when the standard
2 2
bicarbonate is above normal and negative when the standard bicarbonate is below normal.
N = normal; Pco2 = partial pressure of carbon dioxide.

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 which involves a loss of gastric as well as pancreatic, biliary, 75
Table 3-9
and intestinal secretions, vomiting with an obstructed pylorus
Etiology of metabolic acidosis results only in the loss of gastric fluid, which is high in chloride
Increased Anion Gap Metabolic Acidosis and hydrogen, and therefore results in a hypochloremic alkalo-

CHAPTER 3
Exogenous acid ingestion sis. Initially the urinary bicarbonate level is high in compensa-
  Ethylene glycol tion for the alkalosis. Hydrogen ion reabsorption also ensues,
 Salicylate with an accompanied potassium ion excretion. In response to
 Methanol the associated volume deficit, aldosterone-mediated sodium
Endogenous acid production reabsorption increases potassium excretion. The resulting hypo-
 Ketoacidosis kalemia leads to the excretion of hydrogen ions in the face of

Fluid and Electrolyte Management of the Surgical Patient

  Lactic acidosis alkalosis, a paradoxic aciduria. Treatment includes replacement
  Renal insufficiency of the volume deficit with isotonic saline and then potassium
replacement once adequate urine output is achieved.
Normal Anion Gap
Respiratory Derangements.  Under normal circumstances
Acid administration (HCl)
blood Pco2 is tightly maintained by alveolar ventilation,
Loss of bicarbonate
controlled by the respiratory centers in the pons and medulla
GI losses (diarrhea, fistulas)
oblongata.
Ureterosigmoidostomy
Renal tubular acidosis Respiratory Acidosis  Respiratory acidosis is associated with
Carbonic anhydrase inhibitor 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
inhibitor acetazolamide also causes bicarbonate loss from the at the underlying cause. Measures to ensure adequate ventila-
kidneys. tion are also initiated. This may entail patient-initiated volume
Metabolic Alkalosis  Normal acid-base homeostasis prevents expansion using noninvasive bilevel positive airway pressure
metabolic alkalosis from developing unless both an increase in or may require endotracheal intubation to increase minute ven-
bicarbonate generation and impaired renal excretion of bicar- tilation. In the chronic form of respiratory acidosis, the partial
bonate occur (Table 3-10). Metabolic alkalosis results from the pressure of arterial CO2 remains elevated and the bicarbonate
loss of fixed acids or the gain of bicarbonate and is worsened concentration rises slowly as renal compensation occurs.
by potassium depletion. The majority of patients also will have Respiratory Alkalosis  In the surgical patient, most cases of
hypokalemia, because extracellular potassium ions exchange respiratory alkalosis are acute and secondary to alveolar hyper-
with intracellular hydrogen ions and allow the hydrogen ions to ventilation. Causes include pain, anxiety, and neurologic dis-
buffer excess HCO3–. Hypochloremic and hypokalemic meta- orders, including central nervous system injury and assisted
bolic alkalosis can occur from isolated loss of gastric contents ventilation. Drugs such as salicylates, fever, gram-negative
in infants with pyloric stenosis or adults with duodenal ulcer bacteremia, thyrotoxicosis, and hypoxemia are other possibili-
disease. Unlike vomiting associated with an open pylorus, 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
Table 3-10
the underlying cause, but direct treatment of the hyperventila-
Etiology of metabolic alkalosis tion using controlled ventilation may also be required.
Increased bicarbonate generation
1.  Chloride losing (urinary chloride >20 mEq/L)
Mineralocorticoid excess Table 3-11
Profound potassium depletion Etiology of respiratory acidosis: hypoventilation
2.  Chloride sparing (urinary chloride <20 mEq/L)
Loss from gastric secretions (emesis or nasogastric Narcotics
 suction) Central nervous system injury
Diuretics Pulmonary: significant
3.  Excess administration of alkali  Secretions
Acetate in parenteral nutrition  Atelectasis
Citrate in blood transfusions   Mucus plug
Antacids  Pneumonia
Bicarbonate   Pleural effusion
Milk-alkali syndrome Pain from abdominal or thoracic injuries or incisions
Limited diaphragmatic excursion from intra-abdominal
Impaired bicarbonate excretion pathology
1.  Decreased glomerular filtration   Abdominal distention
2. Increased bicarbonate reabsorption (hypercarbia or   Abdominal compartment syndrome
  potassium depletion)  Ascites

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 76 Table 3-12
Electrolyte solutions for parenteral administration

Electrolyte Composition (mEq/L)

PART I

Solution Na Cl K HCO3− Ca Mg mOsm

Extracellular fluid 142 103 4 27 5 3 280–310
Lactated Ringer’s 130 109 4 28 3 273
BASIC CONSIDERATIONS

0.9% Sodium chloride 154 154 308

D5 0.45% Sodium chloride 77 77 407
D5W 253
3% Sodium chloride 513 513 1026
D5 = 5% dextrose; D5W = 5% dextrose in water.

FLUID AND ELECTROLYTE THERAPY Alternative Resuscitative Fluids

A number of alternative solutions for volume expansion and
Parenteral Solutions resuscitation are available (Table 3-13).24 Hypertonic saline
A number of commercially available electrolyte solutions are solutions (3.5% and 5%) are used for correction of
available for parenteral administration. The most commonly 5 severe sodium deficits and are discussed elsewhere in
used solutions are listed in Table 3-12. The type of fluid admin- this chapter. Hypertonic saline (7.5%) has been used as a treat-
istered depends on the patient’s volume status and the type of ment modality in patients with closed head injuries. It has been
concentration or compositional abnormality present. Both lac- shown to increase cerebral perfusion and decrease intracranial
tated Ringer’s solution and normal saline are considered isotonic pressure, thus decreasing brain edema.25 However, there have
and are useful in replacing GI losses and correcting extracellular also been concerns about increased bleeding, because hyper-
volume deficits. Lactated Ringer’s is slightly hypotonic in that tonic saline is an arteriolar vasodilator. A trial of 853 patients
it contains 130 mEq of lactate. Lactate is used rather than bicar- receiving hypertonic saline versus hypertonic saline/dextran
bonate because it is more stable in IV fluids during storage. It 70 vs. 0.9% saline as initial resuscitation in the field showed
is converted into bicarbonate by the liver after infusion, even a higher 28-day mortality in both hypertonic saline groups
in the face of hemorrhagic shock. Evidence has suggested that compared to 0.9% saline.26 Colloids also are used in surgical
resuscitation using lactated Ringer’s may be deleterious because patients, and their effectiveness as volume expanders com-
it activates the inflammatory response and induces apoptosis. pared with isotonic crystalloids has long been debated. Due
The component that has been implicated is the D isomer of lac- to their molecular weight, they are confined to the intravas-
tate, which unlike the L isomer is not a normal intermediary in cular space, and their infusion results in more efficient tran-
mammalian metabolism.22 However, subsequent in vivo stud- sient plasma volume expansion. However, under conditions of
ies showed significantly lower levels of apoptosis in lung and
liver tissue after resuscitation with any of the various Ringer’s
formulations.23
Sodium chloride is mildly hypertonic, containing 154 mEq
of sodium that is balanced by 154 mEq of chloride. The high Table 3-13
chloride concentration imposes a significant chloride load on Alternative resuscitative fluids
the kidneys and may lead to a hyperchloremic metabolic acido-
sis. Sodium chloride is an ideal solution, however, for correcting Molecular Osmolality Sodium
volume deficits associated with hyponatremia, hypochloremia, Solution Weight (mOsm/L) (mEq/L)
and metabolic alkalosis.
Hypertonic saline — 2565 1283
The less concentrated sodium solutions, such as 0.45%
(7.5%)
sodium chloride, are useful for replacement of ongoing GI
losses as well as for maintenance fluid therapy in the post- Albumin 5% 70,000 300 130–160
operative period. This solution provides sufficient free water Albumin 25% 70,000 1500 130–160
for insensible losses and enough sodium to aid the kidneys in Dextran 40 40,000 308 154
adjustment of serum sodium levels. The addition of 5% dextrose
Dextran 70 70,000 308 154
(50 g of dextrose per liter) supplies 200 kcal/L, and dextrose is
always added to solutions containing <0.45% sodium chloride Hetastarch 450,000 310 154
to maintain osmolality and thus prevent the lysis of red blood Hextend 670,000 307 143
cells that may occur with rapid infusion of hypotonic fluids. The Gelofusine 30,000 NA 154
addition of potassium is useful once adequate renal function and
NA = not available.
urine output are established.

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severe hemorrhagic shock, capillary membrane permeability Correction of Life-Threatening Electrolyte 77
increases; this permits colloids to enter the interstitial space,
Abnormalities
which can worsen edema and impair tissue oxygenation. The
theory that these high molecular weight agents “plug” capil- Sodium

CHAPTER 3
lary leaks, which occur during neutrophil-mediated organ injury, Hypernatremia  Treatment of hypernatremia usually consists of
has not been confirmed.27,28 Four major types of colloids are treatment of the associated water deficit. In hypovolemic patients,
available—albumin, dextrans, hetastarch, and gelatins—that volume should be restored with normal saline before the concen-
are described by their molecular weight and size in Table 3-13. tration abnormality is addressed. Once adequate volume has been
Colloid solutions with smaller particles and lower molecular achieved, the water deficit is replaced using a hypotonic fluid
weights exert a greater oncotic effect but are retained within such as 5% dextrose, 5% dextrose in ¼ normal saline, or enterally

Fluid and Electrolyte Management of the Surgical Patient

the circulation for a shorter period of time than larger and administered water. The formula used to estimate the amount of
higher molecular weight colloids. water required to correct hypernatremia is as follows:
Albumin (molecular weight 70,000) is prepared from
heat-sterilized pooled human plasma. It is typically avail- serum sodium − 140
able as either a 5% solution (osmolality of 300 mOsm/L) or Water deficit (L) = × TBW
140
25% solution (osmolality of 1500 mOsm/L). Because it is a
derivative of blood, it can be associated with allergic reactions.
Estimate TBW as 50% of lean body
Albumin has been shown to induce renal failure and impair
mass in men and 40% in women
pulmonary function when used for resuscitation in hemor-
rhagic shock.29 The rate of fluid administration should be titrated to
Dextrans are glucose polymers produced by bacteria achieve a decrease in serum sodium concentration of no more
grown on sucrose media and are available as either 40,000 or than 1 mEq/h and 12 mEq/d for the treatment of acute symp-
70,000 molecular weight solutions. They lead to initial volume tomatic hypernatremia. Even slower correction should be under-
expansion due to their osmotic effect but are associated with taken for chronic hypernatremia (0.7 mEq/h), because overly
alterations in blood viscosity. Thus dextrans are used primar- rapid correction can lead to cerebral edema and herniation. The
ily to lower blood viscosity rather than as volume expanders. type of fluid used depends on the severity and ease of correc-
Dextrans have been used, in association with hypertonic saline, tion. Oral or enteral replacement is acceptable in most cases,
to help maintain intravascular volume. or IV replacement with half- or quarter-normal saline can be
Hydroxyethyl starch solutions are another group of alter- used. Caution also should be exercised when using 5% dextrose
native plasma expanders and volume replacement solutions. in water to avoid overly rapid correction. Frequent neurologic
Hetastarches are produced by the hydrolysis of insoluble amy- evaluation as well as frequent evaluation of serum sodium levels
lopectin, followed by a varying number of substitutions of also should be performed. Hypernatremia is less common than
hydroxyl groups for carbon groups on the glucose molecules. hyponatremia, but has a worse prognosis, and is an independent
The molecular weights can range from 1000 to 3,000,000. predictor of mortality in critical illness.38
The high molecular weight hydroxyethyl starch hetastarch,
Hyponatremia  Most cases of hyponatremia can be treated
which comes as a 6% solution, is the only hydroxyethyl starch
by free water restriction and, if severe, the administration of
approved for use in the United States. Administration of hetas-
sodium. In patients with normal renal function, symptomatic
tarch can cause hemostatic derangements related to decreases
hyponatremia usually does not occur until the serum sodium
in von Willebrand’s factor and factor VIII:C, and its use has
level is ≤120 mEq/L. If neurologic symptoms are present, 3%
been associated with postoperative bleeding in cardiac and neu-
normal saline should be used to increase the sodium by no
rosurgery patients.30,31 Hetastarch also can induce renal dys-
more than 1 mEq/L per hour until the serum sodium level
function in patients with septic shock and was associated with
reaches 130 mEq/L or neurologic symptoms are improved.
a significant increased risk of mortality and acute kidney injury
Correction of asymptomatic hyponatremia should increase the
in the critically ill.32,33 Currently, hetastarch has a limited role
sodium level by no more than 0.5 mEq/L per hour to a maxi-
in massive resuscitation because of the associated coagulopa-
mum increase of 12 mEq/L per day, and even more slowly in
thy and hyperchloremic acidosis (due to its high chloride con-
chronic hyponatremia. The rapid correction of hyponatremia
tent). Hextend is a modified, balanced, high molecular weight
can lead to pontine myelinolysis,39 with seizures, weakness,
hydroxyethyl starch that is suspended in a lactate-buffered solu-
paresis, akinetic movements, and unresponsiveness, and may
tion, rather than in saline. A phase III clinical study comparing
result in permanent brain damage and death. Serial magnetic
Hextend to a similar 6% hydroxyethyl starch in patients under-
resonance imaging may be necessary to confirm the diagnosis.40
going major abdominal surgery demonstrated no adverse effects
on coagulation with Hextend other than the known effects of Potassium
hemodilution.34 Hextend has not been tested for use in mas- Hyperkalemia  Treatment options for symptomatic hyperka-
sive resuscitation, and not all clinical studies show consistent lemia are listed in Table 3-14. The goals of therapy include
results.35 reducing the total body potassium, shifting potassium from
Gelatins are the fourth group of colloids and are produced the extracellular to the intracellular space, and protecting the
from bovine collagen. The two major types are urea-linked cells from the effects of increased potassium. For all patients,
gelatin and succinylated gelatin (modified fluid gelatin, Gelo- exogenous sources of potassium should be removed, including
fusine). Gelofusine has been used abroad with mixed results.36 potassium supplementation in IV fluids and enteral and paren-
Like many other artificial plasma volume expanders, it has teral solutions. Potassium can be removed from the body using
been shown to impair whole blood coagulation time in human a cation-exchange resin such as Kayexalate that binds potas-
volunteers.37 sium in exchange for sodium. It can be administered either

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 78 Hypocalcemia will be refractory to treatment if coexisting hypo-
Table 3-14
magnesemia is not corrected first. Routine calcium supplementa-
Treatment of symptomatic hyperkalemia tion is no longer recommended in association with massive blood
Potassium removal transfusions.41
 Kayexalate Phosphorus
PART I

  Oral administration is 15–30 g in 50–100 mL of 20% Hyperphosphatemia  Phosphate binders such as sucralfate
 sorbitol or aluminum-containing antacids can be used to lower serum
   Rectal administration is 50 g in 200 mL of 20% sorbitol phosphorus levels. Calcium acetate tablets also are useful when
 Dialysis hypocalcemia is simultaneously present. Dialysis usually is
BASIC CONSIDERATIONS

Shift potassium reserved for patients with renal failure.

  Glucose 1 ampule of D50 and regular insulin 5–10 units IV Hypophosphatemia  Depending on the level of depletion and
  Bicarbonate 1 ampule IV tolerance to oral supplementation, a number of enteral and par-
enteral repletion strategies are effective for the treatment of
Counteract cardiac effects hypophosphatemia (see Table 3-15).
  Calcium gluconate 5–10 mL of 10% solution
Magnesium
D50 = 50% dextrose.
Hypermagnesemia  Treatment for hypermagnesemia consists
of measures to eliminate exogenous sources of magnesium,
correct concurrent volume deficits, and correct acidosis if pres-
orally, in alert patients, or rectally. Immediate measures also ent. To manage acute symptoms, calcium chloride (5 to 10 mL)
should include attempts to shift potassium intracellularly with should be administered to immediately antagonize the cardiovas-
glucose and bicarbonate infusion. Nebulized albuterol (10 to cular effects. If elevated levels or symptoms persist, hemodialy-
20 mg) may also be used. Use of glucose alone will cause a sis may be necessary.
rise in insulin secretion, but in the acutely ill, this response Hypomagnesemia  Correction of magnesium depletion can
may be blunted, and therefore both glucose and insulin may be be oral if asymptomatic and mild. Otherwise, IV repletion is
necessary. Circulatory overload and hypernatremia may result indicated and depends on severity (see Table 3-15) and clini-
from the administration of Kayexalate and bicarbonate, so care cal symptoms. For those with severe deficits (<1.0 mEq/L) or
should be exercised when administering these agents to patients those who are symptomatic, 1 to 2 g of magnesium sulfate may
with fragile cardiac function. When ECG changes are pres- be administered IV over 15 minutes. Under ECG monitoring, it
ent, calcium chloride or calcium gluconate (5–10 mL of 10% may be given over 2 minutes if necessary to correct torsades de
solution) should be administered immediately to counteract the pointes (irregular ventricular rhythm). Caution should be taken
myocardial effects of hyperkalemia. Calcium infusion should be when giving large amounts of magnesium, because magnesium
used cautiously in patients receiving digitalis, because digitalis toxicity may develop. The simultaneous administration of cal-
toxicity may be precipitated. All of the aforementioned mea- cium gluconate will counteract the adverse side effects of a rap-
sures are temporary, lasting from 1 to approximately 4 hours. idly rising magnesium level and correct hypocalcemia, which is
Dialysis should be considered in severe hyperkalemia when frequently associated with hypomagnesemia.
conservative measures fail.
Hypokalemia  Treatment for hypokalemia consists of potas- Preoperative Fluid Therapy
sium repletion, the rate of which is determined by the symptoms The administration of maintenance fluids should be all that is
(Table 3-15). Oral repletion is adequate for mild, asymptomatic required in an otherwise healthy individual who may be under
hypokalemia. If IV repletion is required, usually no more than orders to receive nothing by mouth for some period before the
10 mEq/h is advisable in an unmonitored setting. This amount time of surgery. This does not, however, include replenishment
can be increased to 40 mEq/h when accompanied by continu- of a pre-existing deficit or ongoing fluid losses. The follow-
ous ECG monitoring, and even more in the case of imminent ing is a frequently used formula for calculating the volume of
cardiac arrest from a malignant arrhythmia-associated hypoka- maintenance fluids in the absence of pre-existing abnormalities:
lemia. Caution should be exercised when oliguria or impaired
renal function is coexistent. For the first 0–10 kg Give 100 mL/kg per day
Calcium For the next 10–20 kg Give an additional 50 mL/
Hypercalcemia  Treatment is required when hypercalcemia is kg per day
symptomatic, which usually occurs when the serum level exceeds For weight >20 kg Give an additional 20 mL/
12 mg/dL. The critical level for serum calcium is 15 mg/dL, when kg per day
symptoms noted earlier may rapidly progress to death. The ini-
tial treatment is aimed at repleting the associated volume deficit For example, a 60-kg female would receive a total of
and then inducing a brisk diuresis with normal saline. Treatment 2300 mL of fluid daily: 1000 mL for the first 10 kg of body
of hypercalcemia associated with malignancies is discussed weight (10 kg × 100 mL/kg per day), 500 mL for the next 20 kg
later in this chapter. (10 kg × 50 mL/kg per day), and 800 mL for the last 40 kg (40 kg
Hypocalcemia  Asymptomatic hypocalcemia can be treated × 20 mL/kg per day).
with oral or IV calcium (see Table 3-15). Acute symptomatic
hypocalcemia should be treated with IV 10% calcium gluconate An alternative approach is to replace the calculated daily
to achieve a serum concentration of 7 to 9 mg/dL. Associated water losses in urine, stool, and insensible loss with a hypo-
deficits in magnesium, potassium, and pH must also be corrected. tonic saline solution rather than water alone, which allows

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Table 3-15 79

Electrolyte replacement therapy protocol

Potassium

CHAPTER 3
Serum 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 protocol

Fluid and Electrolyte Management of the Surgical Patient

Magnesium
Magnesium 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 d
Magnesium 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 d
If patient has gastric access and needs a bowel regimen:
  Milk of magnesia 15 mL (approximately 49 mEq magnesium) q24h per gastric tube; hold for diarrhea
Calcium
Ionized 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 d
Phosphate
Phosphate 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 d
Phosphate 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 dose
3 mmol KPHO4 = 3 mmol Phos and 4.4 mEq K+ = 1 mL
3 mmol NaPO4 = 3 mmol Phos and 4 mEq Na+ = 1 mL
Neutra-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.

the kidney some sodium excess to adjust for concentration. deficit is primarily clinical (see Table 3-2), although the physi-
Although there should be no “routine” maintenance fluid orders, cal signs may vary with the duration of the deficit. Cardiovascu-
both of these methods would yield an appropriate choice of lar signs of tachycardia and orthostasis predominate with acute
5% dextrose in 0.45% sodium chloride at 100 mL/h as initial volume loss, usually accompanied by oliguria and hemoconcen-
therapy, with potassium added for patients with normal renal tration. Acute volume deficits should be corrected as much as
function. However, many surgical patients have volume and/or possible before the time of operation.
electrolyte abnormalities associated with their surgical disease. Once a volume deficit is diagnosed, prompt fluid replace-
Preoperative evaluation of a patient’s volume status and pre- ment should be instituted, usually with an isotonic crystalloid,
existing electrolyte abnormalities is an important part of over- depending on the measured serum electrolyte values. Patients
all preoperative assessment and care. Volume deficits should with cardiovascular signs of volume deficit should receive a
be considered in patients who have obvious GI losses, such as bolus of 1 to 2 L of isotonic fluid followed by a continuous infu-
through emesis or diarrhea, as well as in patients with poor oral sion. Close monitoring during this period is imperative. Resus-
intake secondary to their disease. Less obvious are those fluid citation should be guided by the reversal of the signs of volume
losses known as third-space or nonfunctional ECF losses that deficit, such as restoration of acceptable values for vital signs,
occur with GI obstruction, peritoneal or bowel inflammation, maintenance of adequate urine output (½–1 mL/kg per hour in
ascites, crush injuries, burns, and severe soft tissue infections an adult), and correction of base deficit. Patients whose volume
such as necrotizing fasciitis. The diagnosis of an acute volume deficit is not corrected after this initial volume challenge and

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 80 those with impaired renal function and the elderly should be exists, particularly in patients with renal or cardiac dysfunction,
considered for more intensive monitoring in an intensive care a central venous catheter or Swan-Ganz catheter may be inserted
unit setting. In these patients, early invasive monitoring of cen- to help guide fluid therapy. After the initial 24 to 48 hours, flu-
tral venous pressure or cardiac output may be necessary. ids can be changed to 5% dextrose in 0.45% saline in patients
If symptomatic electrolyte abnormalities accompany vol- unable to tolerate enteral nutrition. If normal renal function and
PART I

ume deficit, the abnormality should be corrected to the point adequate urine output are present, potassium may be added to
that the acute symptom is relieved before surgical interven- the IV fluids. Daily fluid orders should begin with assessment of
tion. For correction of severe hypernatremia associated with a the patient’s volume status and assessment of electrolyte abnor-
volume deficit, an unsafe rapid fall in extracellular osmolarity malities. There is rarely a need to check electrolyte levels in the
from 5% dextrose infusion is avoided by slowly correcting the first few days of an uncomplicated postoperative course. How-
BASIC CONSIDERATIONS

hypernatremia with 0.45% saline or even lactated Ringer’s solu- ever, postoperative diuresis may require attention to replace-
tion rather than 5% dextrose alone. This will safely and slowly ment of urinary potassium loss. All measured losses, including
correct the hypernatremia while also correcting the associated losses through vomiting, nasogastric suctioning, drains, and
volume deficit. urine output, as well as insensible losses, are replaced with the
appropriate parenteral solutions as previously reviewed.
Intraoperative Fluid Therapy
With the induction of anesthesia, compensatory mechanisms are Special Considerations for the
lost, and hypotension will develop if volume deficits are not Postoperative Patient
appropriately corrected before the time of surgery. Hemody- Volume excess is a common disorder in the postoperative period.
namic instability during anesthesia is best avoided by correct- The administration of isotonic fluids in excess of actual needs
ing known fluid losses, replacing ongoing losses, and providing may result in excess volume expansion. This may be due to the
adequate maintenance fluid therapy preoperatively. In addi- overestimation of third-space losses or to ongoing GI losses that
tion to measured blood loss, major open abdominal surgeries are difficult to measure accurately. The earliest sign of volume
are associated with continued extracellular losses in the form overload is weight gain. The average postoperative patient who
of bowel wall edema, peritoneal fluid, and the wound edema is not receiving nutritional support should lose approximately
during surgery. Large soft tissue wounds, complex fractures 0.25 to 0.5 lb/d (0.11 to 0.23 kg/d) from catabolism. Additional
with associated soft tissue injury, and burns are all associated signs of volume excess may also be present as listed in Table 3-2.
with additional third-space losses that must be considered in the Peripheral edema may not necessarily be associated with intra-
operating room. These represent distributional shifts, in that the vascular volume overload, because overexpansion of total ECF
functional volume of ECF is reduced but fluid is not externally may exist in association with a deficit in the circulating plasma
lost from the body. These functional losses have been referred volume.
to as parasitic losses, sequestration, or third-space edema, Volume deficits also can be encountered in surgical
because the lost volume no longer participates in the normal patients if preoperative losses were not completely corrected,
functions of the ECF. intraoperative losses were underestimated, or postoperative
Until the 1960s saline solutions were withheld during sur- losses were greater than appreciated. The clinical manifestations
gery. Administered saline was retained and was felt to be an are described in Table 3-2 and include tachycardia, orthostasis,
inappropriate challenge to a physiologic response of intraopera- and oliguria. Hemoconcentration also may be present. Treat-
tive salt intolerance. Basic and clinical research began to change ment will depend on the amount and composition of fluid lost.
this concept,42,43 eventually leading to the current concept that In most cases of volume depletion, replacement with an isotonic
saline administration is necessary to restore the obligate ECF fluid will be sufficient while alterations in concentration
losses noted earlier. Although no accurate formula can predict 6 and composition are being evaluated.
intraoperative fluid needs, replacement of ECF during surgery
often requires 500 to 1000 mL/h of a balanced salt solution to ELECTROLYTE ABNORMALITIES IN SPECIFIC
support homeostasis. The addition of albumin or other colloid-
containing solutions to intraoperative fluid therapy is not neces-
SURGICAL PATIENTS
sary. Manipulation of colloid oncotic forces by albumin infusion
during major vascular surgery showed no advantage in support- Neurologic Patients
ing cardiac function or avoiding the accumulation of extravas- Syndrome of Inappropriate Secretion of Antidiuretic
cular lung water.44 Hormone.  The syndrome of inappropriate secretion of antidi-
uretic hormone (SIADH) can occur after head injury or surgery
Postoperative Fluid Therapy to the central nervous system, but it also is seen in association
Postoperative fluid therapy should be based on the patient’s with administration of drugs such as morphine, nonsteroidals,
current estimated volume status and projected ongoing fluid and oxytocin, and in a number of pulmonary and endocrine
losses. Any deficits from either preoperative or intraoperative diseases, including hypothyroidism and glucocorticoid defi-
losses should be corrected, and ongoing requirements should ciency. Additionally, it can be seen in association with a number
be included along with maintenance fluids. Third-space losses, of malignancies, most often small cell cancer of the lung but
although difficult to measure, should be included in fluid also pancreatic carcinoma, thymoma, and Hodgkin’s dis-
replacement strategies. In the initial postoperative period, an 7 ease.45 SIADH should be considered in patients who are
isotonic solution should be administered. The adequacy of euvolemic and hyponatremic with elevated urine sodium levels
resuscitation should be guided by the restoration of acceptable and urine osmolality. ADH secretion is considered inappropriate
values for vital signs and urine output and, in more complicated when it is not in response to osmotic or volume-related condi-
cases, by the correction of base deficit or lactate. If uncertainty tions. Correction of the underlying problem should be attempted

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when possible. In most cases, restriction of free water will improve Acute Renal Failure Patients 81
the hyponatremia. The goal is to achieve net water balance while A number of fluid and electrolyte abnormalities are specific to
avoiding volume depletion that may compromise renal function. patients with acute renal failure. With the onset of renal fail-
Furosemide also can be used to induce free water loss. If hypo- ure, an accurate assessment of volume status must be made. If

CHAPTER 3
natremia persists after fluid restriction, the addition of isotonic or prerenal azotemia is present, prompt correction of the underly-
hypertonic fluids may be effective. The administration of isotonic ing volume deficit is mandatory. Once acute tubular necrosis
saline may sometimes worsen the problem if the urinary sodium is established, measures should be taken to restrict daily fluid
concentration is higher than the infused sodium concentration. intake to match urine output and insensible and GI losses. Oli-
The use of loop diuretics may be helpful in this situation by pre- guric renal failure requires close monitoring of serum potas-
venting further urine concentration. In chronic SIADH, when sium levels. Measures to correct hyperkalemia as reviewed in

Fluid and Electrolyte Management of the Surgical Patient

long-term fluid restriction is difficult to maintain or is ineffective, Table 3-14 should be instituted early, including consideration
demeclocycline and lithium can be used to induce free water loss. of early hemodialysis. Hyponatremia is common in established
Diabetes Insipidus.  Diabetes insipidus (DI) is a disorder of renal failure as a result of the breakdown of proteins, carbohy-
ADH stimulation and is manifested by dilute urine in the case of drates, and fats, as well the administration of free water. Dialy-
hypernatremia. Central DI results from a defect in ADH secre- sis may be required for severe hyponatremia. Hypocalcemia,
tion, and nephrogenic DI results from a defect in end-organ hypermagnesemia, and hyperphosphatemia also are associated
responsiveness to ADH. Central DI is frequently seen in asso- with acute renal failure. Hypocalcemia should be verified by
ciation with pituitary surgery, closed head injury, and anoxic measuring ionized calcium, because many patients also are
encephalopathy.46 Nephrogenic DI occurs in association with hypoalbuminemic. Phosphate binders can be used to control
hypokalemia, administration of radiocontrast dye, and use of hyperphosphatemia, but dialysis may be required in more severe
certain drugs such as aminoglycosides and amphotericin B. In cases. Metabolic acidosis is commonly seen with renal failure,
patients tolerating oral intake, volume status usually is normal as the kidneys lose their ability to clear acid by-products. Bicar-
because thirst stimulates increased intake. However, volume bonate can be useful, but dialysis often is needed. Although
depletion can occur rapidly in patients incapable of oral intake. dialysis may be either intermittent or continuous, renal recovery
The diagnosis can be confirmed by documenting a paradoxical may be improved by continuous renal replacement.50
increase in urine osmolality in response to a period of water
deprivation. In mild cases, free water replacement may be Cancer Patients
adequate therapy. In more severe cases, vasopressin can be Fluid and electrolyte abnormalities are common in patients with
added. The usual dosage of vasopressin is 5 U subcutaneously cancer. The causes may be common to all patient populations or
every 6 to 8 hours. However, serum electrolytes and osmolality may be specific to cancer patients and their treatment.51 Hypo-
should be monitored to avoid excess vasopressin administration natremia is frequently hypovolemic due to renal loss of sodium
with resulting iatrogenic SIADH. caused by diuretics or salt-wasting nephropathy as seen with
some chemotherapeutic agents such as cisplatin. Cerebral salt
Cerebral Salt Wasting.  Cerebral salt wasting is a diagnosis wasting also can occur in patients with intracerebral lesions.
of exclusion that occurs in patients with a cerebral lesion and Normovolemic hyponatremia may occur in association with
renal wasting of sodium and chloride with no other identifiable SIADH from cervical cancer, lymphoma, and leukemia, or
cause.47 Natriuresis in a patient with a contracted extracellular from certain chemotherapeutic agents. Hypernatremia in can-
volume should prompt the possible diagnosis of cerebral salt cer patients most often is due to poor oral intake or GI volume
wasting. Hyponatremia is frequently observed but is nonspecific losses, which are common side effects of chemotherapy. Central
and occurs as a secondary event, which differentiates it from DI also can lead to hypernatremia in patients with central ner-
SIADH. vous system lesions.
Hypokalemia can develop from GI losses associated with
Malnourished Patients: Refeeding Syndrome diarrhea caused by radiation enteritis or chemotherapy, or from
Refeeding syndrome is a potentially lethal condition that can tumors such as villous adenomas of the colon. Tumor lysis syn-
occur with rapid and excessive feeding of patients with severe drome can precipitate severe hyperkalemia from massive tumor
underlying malnutrition due to starvation, alcoholism, delayed cell destruction.
nutritional support, anorexia nervosa, or massive weight loss Hypocalcemia can be seen after removal of a thyroid or
in obese patients.48 With refeeding, a shift in metabolism from parathyroid tumor or after a central neck dissection, which can
fat to carbohydrate substrate stimulates insulin release, which damage the parathyroid glands. Hungry bone syndrome produces
results in the cellular uptake of electrolytes, particularly phos- acute and profound hypocalcemia after parathyroid surgery for
phate, magnesium, potassium, and calcium. However, severe secondary or tertiary hyperparathyroidism because calcium is
hyperglycemia may result from blunted basal insulin secretion. rapidly taken up by bones. Prostate and breast cancer can result
The refeeding syndrome can be associated with enteral or par- in increased osteoblastic activity, which decreases serum calcium
enteral refeeding, and symptoms from electrolyte abnormalities by increasing bone formation. Acute hypocalcemia also can occur
include cardiac arrhythmias, confusion, respiratory failure, and with hyperphosphatemia, because phosphorus complexes with
even death. To prevent the development of refeeding syndrome, calcium. Hypomagnesemia is a side effect of ifosfamide and
underlying electrolyte and volume deficits should be corrected. cisplatin therapy. Hypophosphatemia can be seen in hyperpara-
Additionally, thiamine should be administered before the initia- thyroidism, due to decreased phosphorus reabsorption, and in
tion of feeding. Caloric repletion should be instituted slowly and oncogenic osteomalacia, which increases the urinary excretion of
should gradually increase over the first week.49 Vital signs, fluid phosphorus. Other causes of hypophosphatemia in cancer patients
balance, and electrolytes should be closely monitored and any include renal tubular dysfunction from multiple myeloma,
deficits corrected as they evolve. Bence Jones proteins, and certain chemotherapeutic agents.

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 82 Acute hypophosphatemia can occur as rapidly proliferating   2. Bourque CW, Oliet SHR. Osmoreceptors in the central ner-
malignant cells take up phosphorus in acute leukemia. Tumor vous system. Annu Rev Physiol. 1997;59:601.
lysis syndrome or the use of bisphosphonates to treat hypercalce-   3. Verbalis JG. How does the brain sense osmolality? J Am Soc
mia also can result in hyperphosphatemia. Nephrol. 2007;18(12):3056.
Malignancy is the most common cause of hypercalcemia   4. Stauss HM. Baroreceptor reflex function. Am J Physiol Regul
PART I

Integr Comp Physiol. 2002;283:R284.

in hospitalized patients and is due to increased bone resorption
  5. Miller M. Syndromes of excess antidiuretic hormone release.
or decreased renal excretion. Bone destruction occurs from bony Crit Care Clin. 2001;17:11.
metastasis as seen in breast or renal cell cancer but also can   6. Kapoor M, Chan G. Fluid and electrolyte abnormalities. Crit
occur in multiple myeloma. With Hodgkin’s and non-Hodgkin’s Care Clin. 2001;17:571.
lymphoma, hypercalcemia results from increased calcitriol for-  7. Adrogue HJ, Lederer ED, Suki WN, et al. Determinants
BASIC CONSIDERATIONS

mation, which increases both absorption of calcium from the of plasma potassium in diabetic ketoacidosis. Medicine.
GI tract and mobilization from bone. Humoral hypercalcemia 1986;65:163.
of malignancy is a common cause of hypercalcemia in cancer   8. Zietse R, Zuotendijk R, Hoorn EJ. Fluid, electrolyte and acid-
patients. As in primary hyperparathyroidism, a parathyroid- base disorders associated with antibiotic therapy. Nat Rev
related protein is secreted that binds to parathyroid receptors, Nephrol. 2009;5(4):193.
  9. Cobos E, Hall RR. Effects of chemotherapy on the kidney.
stimulating calcium resorption from bone and decreasing renal
Semin Nephrol. 1993;13:297.
excretion of calcium. The treatment of hypercalcemia of malig- 10. Gennari FJ. Hypokalemia. N Engl J Med. 1998;339:451.
nancy should begin with saline volume expansion, which will 11. French S, Subauste J, Geraci S. Calcium abnormalities in hos-
decrease renal reabsorption of calcium as the associated volume pitalized patients. South Med J. 2012;105(4):231.
deficit is corrected. Once an adequate volume status has been 12. Witteveen JE, van Theil S, Romijn JA. Therapy of endo-
achieved, a loop diuretic may be added. Unfortunately, these crine disease: hungry bone syndrome. Eur J Endocrinol.
measures are only temporary, and additional treatment is often 2013;168(3):R45.
necessary. A variety of drugs are available with varying times 13. Bushinsky DA, Monk RD. Calcium. Lancet. 1998;352:306.
of onset, durations of action, and side effects.52 The bisphos- 14. Dunlay RW, Camp MA, Allon M, et al. Calcitriol in prolonged
phonates etidronate and pamidronate inhibit bone resorption hypocalcemia due to tumor lysis syndrome. Ann Intern Med.
and osteoclastic activity. They have a slow onset of action, but 1989;110:162.
15. Reber PM, Heath H. Hypocalcemic emergencies. Med Clin
effects can last for 2 weeks. Calcitonin also is effective, inhibit-
North Am. 1995;19:93.
ing bone resorption and increasing renal excretion of calcium. 16. Tong GM, Rude RK. Magnesium deficiency in critical illness.
It acts quickly, within 2 to 4 hours, but its use is limited by the J Intensive Care Med. 2005;20(1):3.
development of tachyphylaxis. Corticosteroids may decrease 17. Quamme GA. Renal magnesium handling: new insights in
tachyphylaxis in response to calcitonin and can be used alone understanding old problems. Kidney Int. 1997;52:1180.
to treat hypercalcemia. Gallium nitrates are potent inhibitors of 18. Marino PL. Acid-base interpretations. In: Marino PL, ed. The
bone resorption. They display a long duration of action but can ICU Book. 2nd ed. Baltimore: Williams & Wilkins; 1998:581.
cause nephrotoxicity. Mithramycin is an antibiotic that blocks 19. Gluck SL. Acid-base. Lancet. 1998;352:474.
osteoclastic activity, but it can be associated with liver, renal, 20. Kraut JA, Madias NE. Treatment of acute metabolic acidosis: a
and hematologic abnormalities, which limits its use to the pathophysiologic approach. Nat Rev Nephrol. 2012;8(10):589.
21. Pal JD, Victorino GP, Twomey P, et al. Admission serum
treatment of Paget’s disease of bone. For patients with severe,
lactate levels do not predict mortality in the acutely injured
refractory hypercalcemia who are unable to tolerate volume patient. J Trauma. 2006;60:583.
expansion due to pulmonary edema or congestive heart failure, 22. Koustova E, Standon K, Gushchin V, et al. Effects of lactated
dialysis is an option. Ringer’s solution on human leukocytes. J Trauma. 2002;53:782.
Tumor lysis syndrome results when the release of intracel- 23. Shires GT, Browder LK, Steljes TP, et al. The effect of shock
lular metabolites overwhelms the kidneys’ excretory capacity. resuscitation fluids on apoptosis. Am J Surg. 2005;189:85.
This rapid release of uric acid, potassium, and phosphorus can 24. Roberts JS, Bratton SL. Colloid volume expanders: problems,
result in marked hyperuricemia, hyperkalemia, hyperphospha- pitfalls, and possibilities. Drugs. 1998;55:621.
temia, and hypocalcemia, and acute renal failure. It is typically 25. Cottenceau V, Masson F, Mahamid E, et al. Comparison
seen with poorly differentiated lymphomas and leukemias but effects of equiosmolar doses of mannitol and hypertonic saline
also can occur with a number of solid tumor malignancies. on cerebral blood flow and metabolism in traumatic brain
injury. J Neurotrauma. 2011;28(10):2003.
Tumor lysis syndrome most commonly develops during treat-
26. Bulger EM, May S, Kerby JD, et al. Out-of-hospital hyper-
ment with chemotherapy or radiotherapy. Once it develops, tonic resuscitation after traumatic hypovolemic shock: a ran-
volume expansion should be undertaken and any associated domized, placebo-controlled trial. Ann Surg. 2011;253(3):431.
electrolyte abnormalities corrected. In this setting, hypocal- 27. Ley K. Plugging the leaks. Nat Med. 2001;7:1105.
cemia should not be treated unless it is symptomatic to avoid 28. Conhaim RL, Watson KE, Potenza BM, et al. Pulmonary cap-
metastatic calcifications. Dialysis may be required for man- illary sieving of hetastarch is not altered by LPS-induced sep-
agement of impaired renal function or correction of electrolyte sis. J Trauma. 1999;46:800.
abnormalities. 29. Lucas CE. The water of life: a century of confusion. J Am
Coll Surg. 2001;192:86.
30. de Jonge E, Levi M. Effects of different plasma substitutes
REFERENCES on blood coagulation: a comparative review. Crit Care Med.
2001;291:1261.
Entries highlighted in blue are key references.
31. Navickis RJ, Haynes GR, Wilkes MM. Effect of hydroxyethyl
  1. Aloia JF, Vaswani A, Flaster E, et al. Relationship of body starch on bleeding after cardiopulmonary bypass: a meta-
water compartment to age, race and fat-free mass. J Lab Clin analysis of randomized trilals. J Thorac Cardiovasc Surg.
Med. 1998;132:483. 2012;144(4):223.

VRG RELEASE: tahir99

https://kickass.to/user/tahir99/uploads/
32. Schortgen F, Lacherade JC, Bruneel F, et al. Effects of 42. Shires GT, Williams J, Brown F. Acute changes in extracel- 83
hydroxyethylstarch and gelatin on renal function in severe lular fluids associated with major surgical procedures. Ann
sepsis: a multicenter randomized study. Lancet. 2001;357:911. Surg. 1961;154:803.
33. Zarychanski R, Abou-Setta AM, Turgeon AF, et al. Associa- 43. Shires GT, Jackson DE. Postoperative salt tolerance. Arch

CHAPTER 3
tion of hydroxyethyl starch administration with mortality and Surg. 1962;84:703.
acute kidney injury in critically ill patients requiring volume 44. Shires GT III, Peitzman AB, Albert SA, et al. Response
resuscitation: a systematic review and meta-analysis. JAMA. of extravascular lung water to intraoperative fluids. Ann
2013;309(7):678. Surg. 1983;197:515.
34. Gan TJ, Bennett-Guerrero E, Phillips-Bute B, et al. Hextend, 45. Ellison DH, Burl T. Clinical practice. The syndrome of inap-
a physiologically balanced plasma expander for large volume propriate antidiuresis. N Engl J Med. 2007;356(20):2064.
use in major surgery: a randomized phase III clinical trial. 46. Tisdall M, Crocker M, Watkiss J, et al. Disturbances of sodium

Fluid and Electrolyte Management of the Surgical Patient

Anesth Analg. 1999;88:992. in critically ill adult neurologic patients: a clinical review.
35. Boldt J, Haisch G, Suttner S, et al. Effects of a new modified, J Neurosurg Anesthesiol. 2006;18(1):57.
balanced hydroxyethyl starch preparation (Hextend) on mea- 47. Yee AH, Burns JD, Wijdicks EF. Cerebral salt wasting: patho-
sures of coagulation. Br J Anaesth. 2002;89:772. physiology, diagnosis, and treatment. Neurosurg Clin N Am.
36. Rittoo D, Gosling P, Bonnici C, et al. Splanchnic oxygen- 2010;21(2):339.
ation in patients undergoing abdominal aortic aneurysm repair 48. Kozar RA, McQuiggan MM, Moore FA. Nutritional support
and volume expansion with eloHAES. Cardiovasc Surg. in trauma patients. In: Shikora SA, Martindale RG, Schwait-
2002;10:128. zberg SD, eds. Nutritional Considerations in the Intensive
37. Coats TJ, Brazil E, Heron M, et al. Impairment of coagulation Care Unit. 1st ed. Dubuque, IA: Kendall/Hunt Publishing;
by commonly used resuscitation fluids in human volunteers. 2002:229.
Emerg Med J. 2006;23:846. 49. Boateng AA, Sriram K, Mequid MM, et al. Refeeding syn-
38. Overgaard-Steensen C, Ring T. Clinical Review: Practical drome: treatment considerations based on collective analysis
approach to hyponatremia and hypernatremia in critically ill of literature case reports. Nutrition. 2010;26(2):156.
patients. Crit Care. 2013;17(1):206. 50. Glassford NJ, Bellomo R. Acute kidney injury: how can we
39. Norenberg MD. Central pontine myelinolysis: historical and facilitate recovery? Curr Opin Crit Care. 2011;17(6):562.
mechanistic considerations. Metab Brain Dis. 2010;25(1):97. 51. Kapoor M, Chan GZ. Fluid and electrolyte abnormalities. Crit
40. Graff-Radford J, Fugate JE, Kauffmann TJ. Clinical and radio- Care Clin. 2002;17:503.
logic correlations of central pontine myelinolysis syndrome. 52. Clines GA. Mechanisms and treatment of hypercalcemia of
Mayo Clin Proc. 2011;86(11):1063. malignancy. Curr Opin Endocrinol Diabetes Obes. 2011;
41. American College of Surgeons. Shock. In: American College 18(6)339.
of Surgeons Advanced Trauma Life Support Manual. 9th ed.
Chicago: American College of Surgeons; 2012.

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