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

4
Fluid, Electrolyte, and Acid–Base
Disorders in the Surgery Patient
Stephen F. Lowry
Objectives
1. To understand the normal electrolyte composition
of body fluids and how they are modified by
injury and surgical disease.
2. To understand the importance of evaluating fluid
status.
3. To recognize the clinical manifestation of common
electrolyte abnormalities and methods for their
correction.
4. To understand the common manifestation of
acid–base abnormalities.
Cases
Case 1
A 72-year-old man undergoes subtotal colectomy for massive lower GI
bleeding. He receives five units of blood during and following operation and is NPO for 6 days while receiving dextrose 5% in water
(D5/W) at a rate of 125 mL/hour. Urine output remains normal with
specific gravity of 1.012. On the sixth postoperative day, he is disoriented and combative. Among the results of workup are serum sodium
= 119 mEq/L, potassium = 3.6 mEq/L, chloride = 85 mEq/L, glucose =
120 mg/dL, blood urea nitrogen (BUN) = 24.
Case 2
A 40-year-old woman presents with a 1 week history of persistent
upper abdominal pain in association with nausea and vomiting. She
tolerates only small amounts of clear fluids by mouth. No diarrhea
is present. Physical examination is unrevealing except for loss of
skin turgor and reduced breath sounds over the right chest. Lab results include sodium = 138 mEq/L, potassium = 2.6 mEq/L, HCO3 =
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4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
43 mEq/L. A blood gas is obtained, revealing pH = 7.57, Pao2 = 98 mm
Hg, Paco2 = 52 mm Hg, base excess = 10.
Case 3
A 58-year-old woman presents with a 1-week history of confusion,
lethargy, and persistent nausea. She has new complaints of back and
hip pain. Past history includes a mastectomy for breast cancer 5 years
previously. Laboratory values obtained during evaluation include
hematocrit (Hct) = 41, white blood count (WBC) = 9000, platelets =
110,000, sodium = 137 mEq/L, potassium = 3.8 mEq/L, BUN =
25 mg/dL, albumin = 3.4 g/dL, bilirubin = 1.5 g/dL, alkaline phosphatase = 350 IU/L, calcium = 14.2 mg/dL.
Introduction
An understanding of changes in fluid, electrolyte, and acid–base concepts is fundamental to the care of surgical patients. These changes can
range from mild, readily correctable deviations to life-threatening
abnormalities that demand immediate attention. This chapter outlines
some of the physiologic mechanisms that initiate such imbalances and
methods to systematically evaluate the diverse clinical and biochemical data that lead to decisions regarding therapy. The information and
data presented below are intended for application in adult patients,
although the principles espoused also are germane to pediatric
patients.
Basic Concepts
The Stress Response
The normal physiologic response to injury or operation produces a
neuroendocrine response that preserves cellular function and promotes maintenance of circulating volume. This is readily demonstrable in terms of retention of water and sodium and the excretion
of potassium. Many stimuli can produce this response, including many
associated with trauma or operation. Activation of several endocrine
response pathways increases the levels of antidiuretic hormone (ADH),
aldosterone, angiotensin II, cortisol, and catecholamines. Hyperosmolarity and hypovolemia are the principal stimulants for ADH release,
which increases renal water resorption from the collecting ducts and
raises urine osmolarity. Aldosterone, the principal stimulus for renal
potassium excretion, also is increased by angiotensin II, which can
increase both renal sodium and water retention. Aldosterone also is
increased by elevated levels of potassium, a common consequence of
tissue injury. Hydrocortisone and catecholamine release also contribute
to the excretion of potassium.
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S.F. Lowry
Body Fluid Compartments
Total body water (TBW) approximates 60% of body weight (BW) and
is divided among the intracellular volume (ICV) as 40% of BW and an
extracellular volume (ECV) representing 20% of BW. The ECV is
divided further into an interstitial fluid volume (IFV) pool, which is
roughly 15% of BW, and the intravascular or plasma volume (PV),
which approximates 5% of BW. The TBW is the solvent for most of the
solutes in the body, and it is assumed that water moves freely between
the ECV and ICV in an effort to equalize the concentration of solutes
within each space. However, the solute and colloid concentrations of
the ICV and ECV differ markedly. The ECV contains most of the body
sodium, while the predominant ICV cation is potassium. Albumin represents the dominant osmotically active colloid within the ECV and
virtually is excluded from the ICV. The exogenous administration of
electrolytes results in the distribution of that ion to the usual fluid compartment of highest preferential concentration.
Electrolytes
When an electrolyte dissolves in water, it releases positive and negative ions. Although, as noted above, their concentrations vary between
fluid compartments, the distribution of water across fluid compartments seeks to equalize the concentration of total solutes and other
osmotically active particles. When considering electrolyte problems, it
is useful to use the milliequivalent (mEq) measure of their chemical
combining capacity. In some cases, this must be converted from the
weight expression milligram (mg) expressed on the laboratory report.
Table 4.1 assists in this conversion.
A millimole (mM) is the atomic weight of a substance expressed in
milligrams. A milliosmole (mOsm) is a measure of the number of
osmotically active particles in solution. Since mOsm does not depend
on valence, the mM dissolved in solution will be the same as mOsm.
The osmolarity of a solution depends on the number of active particles per unit of volume (mOsm/L). The normal osmolarity of serum is
290 ± 10 mOsm/L. The effective osmolarity (tonicity) involves the mea-
Table 4.1. Data for serum electrolytes.
Normal
Electrolyte
Sodium
Potassium
Calcium
Magnesium
Chloride
Phosphorus
mg/dL
322
17.5
10
2.4
35.7
3.4
mEq/L
140
4.5
5
2
102
2.0
Source: Reprinted from Pemberton LB, Pemberton DK. Treatment of Water, Electrolyte,
and Acid-Base Disorders in the Surgical Patient. New York: McGraw Hill, 1994. With permission of The McGraw-Hill Companies.
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
surement of two solutes, sodium and glucose, that represent nearly
90% of ECV osmolarity. This can be modified by addition of urea concentration, especially in conditions of uremia. The formula for calculating approximate osmolarity is:
POSM = 2 ¥ plasma [Na+] + [glucose]/20 + [BUN]/3
Because water moves freely between fluid compartments, ECV osmolarity (or tonicity) is equivalent to that in the ICV.
Maintenance Requirements
There are several principles that underlie the prescription for replacing
fluid and electrolytes in surgical patients. This includes a knowledge
of normal maintenance requirements as well as replacement for losses.
Water
The normal losses of water include sensible (measurable) losses from
urine (500–1500 mL/day) and feces (100–200 mL/day), as well as
insensible (unmeasurable) loses from sweat and respiration (8–
12 mL/kg/day). Cutaneous insensible losses increase by approximately 10% for each degree C above normal. A method to roughly
calculate daily normal water requirements is shown in Figure 4.1. The
water of biologic oxidation (catabolism) contributes up to 300 mL/day
and can be subtracted from these calculations. For healthy adults, an
estimated daily maintenance fluid requirement approximates 30 to
35 mL/kg/day.
Sodium
Sodium losses in urine can vary widely but, in general, approximate
daily intake. The normal kidney can conserve sodium to a minimum
level of 5 to 10 mEq/L. A figure of 70 to 100 mEq Na/day is a reasonable estimate of maintenance level.
Potassium
The normal excretion of potassium approximates 40 to 60 mEq/day.
Since the renal conservation of potassium is not as efficient as for
sodium, this is the minimum level of daily replacement in healthy
adults (0.5–1.0 mEq/kg/day).
Summary of Normal Maintenance Fluids for Surgical Patients
In the absence of other comorbidities or prolonged injury/operation
induced stress, the NPO surgical patient is adequately maintained
by infusion of variable combinations of dextrose (D5) and saline (up
to 0.5 N) containing solutions, with approximately 15 to 20 mEq/L of
potassium added. The rate of infusion should be adjusted to achieve
water replacement as outlined above. Such parenteral solutions, when
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S.F. Lowry
Total Body Water
[60% Body Wt. (42L)]
INTRACELLULAR
[40% Body Wt. (28L)]
CATIONS
Na+ 12.0 mEq/L
K+ 150 mEq/L
Ca2+ 4.0 mEq/L
Mg2+ 34.0 mEq/L
ANIONS
Cl–
4.0 mEq/L Proteins 54 mEq/L
HCO3– 12.0 mEq/L Other 90 mEq/L
HPO42– , H2PO4– 40 mEq/L
EXTRACELLUAR
[20% Body Wt. (14L)]
CATIONS
Na+ 14.2 mEq/L
K+ 4.3 mEq/L
Ca2+ 2.5 mEq/L
Mg2+ 1.1 mEq/L
ANIONS
Cl–
104.0 mEq/L Proteins 14 mEq/L
Other 5.9 mEq/L
HCO3– 24 mEq/L
HPO42– , H2PO4– 2.0 mEq/L
INTERSTITIAL
(10.5 L)
PLASMA
(3.5 L)
Figure 4.1. Distribution of body water and electrolytes in a healthy 70-kg male. (Adapted from Narins
RG, Krishna GC. Disorders of water balance. In: Stein JH, ed. Internal Medicine, 2nd ed. Philadelphia:
Lippincott Williams & Wilkins. Reprinted from Nathens AB, Maier RV. Perioperative Fluids and Electrolytes. In: Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence.
New York: Springer-Verlag, 2001, with permission.)
given at an appropriate rate of infusion, suffice to manage the majority of postoperative patients.
Perioperative Fluid and Electrolyte Requirements
The management of fluid and electrolytes in the stressed surgical
patient requires a systematic approach to the changing dynamics and
demands of the patient. Consideration of existing maintenance
requirements, deficits or excesses, and ongoing losses requires
regular monitoring and flexibility in prescribing. While the majority
of patients require only minor, if any, adjustments in parenteral fluid
intake, some present challenging and life-threatening situations.
Fluid Sequestration
Following injury or operation, the extravasation of intravascular fluid
into the interstitium leads to tissue edema (“third space”). Estimates of
this volume for general surgery patients range from 4 to 8 mL/kg/h
and this volume may persist for up to 24 hours or longer. This loss of
functional ECV must be considered as an additional ongoing loss in
the early postoperative or injury period.
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
Gastrointestinal Losses
Additional ongoing losses from intestinal drains, stomas, tubes, and
fistulas also must be documented and replaced. The fluid volume and
electrolyte concentration of such losses vary by site and should be
recorded carefully. Replacement of such losses should approximate the
known, or measured, concentration of electrolytes (Table 4.2).
Intraoperative Losses
Careful attention to the operative record for replacement of fluids
during surgery always is warranted. Usually, additional fluids for prolonged operations and for operations upon open cavities is warranted.
Surgeons must know what fluids and medications were given during
the procedure so that they can write appropriate postoperative fluid
orders. Orders for intravenous fluids may need to be rewritten frequently to maintain normal heart rate, urine output (0.5–1.0 mL/kg/h),
and blood pressure.
Defining Problems of Fluid and Electrolyte Imbalance
Fluid balance and electrolyte disorders can be classified into disturbances of (1) extracellular fluid volume; (2) sodium concentration;
and (3) composition (acid–base balance and other electrolytes). When
confronted with an existing problem of fluid or electrolyte derangement, it is helpful initially to analyze the issues of fluid (water) and
electrolyte imbalance separately.
Fluid Status
The initial issue is whether a deficit or excess of water exists. A deficiency of extracellular volume can be diagnosed clinically (Table 4.3).
Acutely, there may be no changes in serum sodium, whereas repeated
studies may demonstrate changes in sodium as well as in BUN.
Table 4.2. Volume and composition of gastrointestinal fluid losses.
Volume
Source
(mL)
Stomach
1000–4200
Duodenum
100–2000
Ileum
1000–3000
Colon
500–1700
(diarrhea)
Bile
500–1000
Pancreas
500–1000
Na+
(mEq/L)
20–120
110
80–150
120
Cl(mEq/L)
130
115
60–100
90
K+
(mEq/L)
10–15
15
10
25
HCO3(mEq/L)
—
10
30–50
45
H+
(mEq/L)
30–100
—
—
—
140
140
100
30
5
5
25
115
—
—
Source: Reprinted from Nathens AB, Maier RV. Perioperative fluids and electrolytes. In:
Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.
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Orthostatic hypotension
Tachycardia
Collapsed veins
Collapsing pulse
Soft small tongue
with longitudinal
wrinkling
Decreased skin turgor
Mild decrease in
temperature
(97°–99°R)
Cardiovascular
Tissue
Metabolic
Marked decrease in
temperature
(95°–98°R)
Atonic muscles
Sunken eyes
Cutaneous lividity
Hypotension
Distant heart sounds
Cold extremities
Absent peripheral pulses
Nausea, vomiting
Refusal to eat
Silent ileus and distention
Severe
Decreased tension reflexes
Anesthesia of distal
extremities
Stupor
Coma
Severe
None
None
Subcutaneous pitting edema
Basilar rales
Elevated venous pressure
Distention of peripheral
veins
Increased cardiac output
Loud heart sounds
Functional murmurs
Bounding pulse
High pulse pressure
Increased pulmonary second
sound
Gallop
None
Anasarca
Moist rales
Vomiting
Diarrhea
Pulmonary edema
At operation:
Edema of stomach, colon, lesser and greater omenta,
and small bowel mesentery
Symptoms of excess
Moderate
None
Source: Reprinted from Shires GT, Shires GT III, Lowry S. Fluid, electrolyte and nutritional management of the surgical patient. In: Schwartz SI, ed. Principles of Surgery,
6th ed. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies.
R = rectal.
Progressive decrease
in food consumption
Gastrointestinal
Type of Sign
Central nervous
system
Symptoms of deficit
Moderate
Sleepiness
Apathy
Slow responses
Anorexia
Cessation of usual
activity
Table 4.3. Extracellular fluid volume.
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S.F. Lowry
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
Under chronic conditions, an assessment of ECV also may be determined from serum sodium level and osmolarity. A high serum sodium
(>145 mEq/L) indicates a water deficit, whereas low serum sodium
(<135 mEq/L) confirms water excess. The sodium level provides no
information about the body sodium content, merely the relative
amounts of free water and sodium. If serum osmolarity is high, it is
important to consider the influence of other osmotically active particles, including glucose. Elevated glucose should be treated and will
restore, at least partially, serum osmolarity.
Water Excess
Although water excess may coexist with either sodium excess or deficit,
the most common postoperative variant, hypo-osmolar hyponatremia,
may develop slowly with minimal symptoms. Rapid development
results in neurologic symptoms that may eventuate in convulsions and
coma if not properly addressed as discussed in Case 1. A serum
sodium less than 125 mEq/L demands immediate attention. Other
causes of hyponatremia are listed in Table 4.4. (See Algorithm 4.1 for
treatment.)
The treatment of water excess involves removing the excess water,
adding sodium, or using both approaches to increase serum osmolarity. Restriction of water intake often suffices in that continued sensible
and insensible losses will assure free water loss. (The amount of excess
water may be estimated by: BW in kg ¥ 0.04 = L of water excess.) In
cases in which sodium administration is necessary (i.e., symptomatic
Table 4.4. Causes of hyponatremia.
Pseudohyponatremia (normal plasma osmolarity)
Hyperlipidemia, hyperproteinemia
Dilutional hyponatremia (increased plasma osmolarity)
Hyperglycemia, mannitol
True hyponatremia (reduced plasma osmolarity)
Reduction in ECF volume
Plasma, GI, skin, or renal losses (diuretics)
Expanded ECF volume
Congestive heart failure
Hypoproteinemic states (cirrhosis, nephrotic syndrome, malnutrition)
Normal ECF volume
SIADH
Pulmonary or CNS lesions
Endocrine disorders (hypothyroidism, hypoadrenalism)
Drugs (e.g., morphine, tricyclic antidepressants, clofibrate,
antineoplastic agents, chlorpropamide, aminophylline, indomethacin)
Miscellaneous (pain, nausea)
SIADH, syndrome of inappropriate antidiuretic hormone secretion.
Source: Reprinted from Nathens AB, Maier RV. Perioperative fluids and electrolytes. In:
Norton JA, Bollinger RR, Chang AE, et al, eds. Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag, 2001, with permission.
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S.F. Lowry
Patient is hyponatremic
Patient is hypernatremic
Rule out artifacts (e.g., from
presence of glucose, mannitol,
or glycine). Suspect renal
dysfunction and acid–base
disorders. Initiate continuous
cardiovascular, renal, and
neurologic monitoring.
Assess volume status.
Assess volume status. Monitor
cardiovascular, renal, and
neurologic function.
Volume is low
Replace volume deficit
with isotonic saline or
lactated Ringer’s solution.
Volume is low
Correct volume deficit:
• Administer isotonic
saline if patient is
alkalotic.
• Administer lactated
Ringer’s solution if
patient is acidotic.
Volume is normal
Volume is increased
Volume is normal
Give diuretics.
Volume is increased
Consider administration
of a loop diuretic.
Evaluate severity of symptoms,
including CNS alterations,
hypotension, and oliguria.
Symptoms are mild
Symptoms are severe
Restrict water intake.
Infuse hypertonic (3%)
saline. Do not raise serum
sodium by more than
12 mEq/L in first 24 hr.
Discontinue infusion when
symptoms improve.
Replace water deficit (no
more than half in first
24 hr; remainder over
1–2 days). Discontinue
infusion when symptoms
improve. If neurogenic
diabetes insipidus is
present, administer
vasopressin.
Algorithm 4.1. Initial assessment of patient with fluid and electrolyte imbalance. (Reprinted from
Van Zee KJ, Lowry SF. Life-threatening electrolyte abnormalities. In: Wilmore DW, Cheung LY, Harken
AH, et al, eds. ACS Surgery: Principles and Practice (Section 1: Resuscitation). New York: WebMD
Corporation, 1997.)
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
hyponatremia), a rise in serum sodium may be achieved by administration of the desired increase of sodium (in mEq/L) = 0.6 (% of BW as
TBW) ¥ BW (in kg). An uncommon but devastating complication of
raising serum sodium too rapidly is central pontine demyelinating syndrome. This may occur if sodium is increased at a rate >0.5 mEq/L per
hour. To prevent this complication, it is generally recommended that
symptomatic patients receive one half of the calculated sodium dose
(using hypertonic sodium solutions, such as 3% saline) over 8 hours to
bring serum sodium into an acceptable range (120–125 mEq/L), as
would be appropriate in Case 1. The remaining dose then may be
infused over the next 16 hours. Do not use hypotonic saline solutions
until the serum sodium is in an acceptable range. Medications that
antagonize ADH effect, such as demeclocycline (300–600 mg b.i.d.), also
may be used cautiously, especially in patients with renal failure.
Water Excess Caused by SIADH
The syndrome of inappropriate ADH (SIADH) results from increased
ADH secretion in the face of hypo-osmolarity and normal blood
volume. The criteria for this diagnosis also include a reduced aldosterone level with urine sodium >20 mEq/L, serum< urine osmolarity,
and the absence of renal failure, hypotension, or edema. The syndrome of inappropriate ADH results from several diseases, including
malignant tumors, central nervous system (CNS) diseases, pulmonary
disorders, medications, and severe stress. The primary treatments for
SIADH are management of the underlying condition and water restriction (<1000 mL/day). Administration of hypotonic fluids should be
avoided.
Water Deficit
A deficit of ECV is the most frequently encountered derangement of
fluid balance in surgical patients. It may occur from shed blood, loss
of gastrointestinal fluids, diarrhea, fistulous drainage, or inadequate
replacement of insensible losses. More subtle are “third-space” losses
(e.g., peritonitis) or sequestration of fluids intraluminally and intramurally (e.g., bowel obstruction). Similar to changes in conditions
of water excess, a severe or rapidly developing deficit of water may
cause several symptoms (Table 4.3). Lab tests for serum sodium
(>145 mEq/L) and osmolarity (>300 mOsm/L) establish the diagnosis.
Water deficit results from loss of hypotonic body fluids without adequate replacement or intake of hypertonic fluids without adequate
sodium excretion. Patients with decreased mental status or those
unable to regulate their water intake are prone to this problem. Patients
who are NPO, cannot swallow, or are receiving water-restricted (hypertonic) nutritional regimens also develop this disorder. Excess water loss
may result from insensible sources (lungs, sweat) or from excessive
gastrointestinal (GI) or renal losses. Large renal losses of hypotonic
urine are referred to as diabetes insipidus (DI), which may be of central
origin (lack of ADH secretion) or renal (reduces concentrating ability).
The most common cause of central DI is trauma. This form often is
reversible. Other causes include infections and tumors of the pituitary
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S.F. Lowry
region. Nephrogenic DI refers to a renal inability to concentrate
urine and can be caused by hypercalcemia, hypokalemia, as well as
drugs such as lithium. Once a diagnosis of water deficit is entertained,
evaluation of urine concentrations can be useful.
While water deficit may be associated with either sodium excess or
deficit (see Algorithm 4.1), the specific treatment of water deficit must
include the administration of free water as a dextrose solution (D5W).
Treatment must be done urgently for serum sodium levels >160 mEq/L.
Up to 1 L of D5W may be given over 2 to 4 hours to correct the
hypernatremia.
Sodium Concentration Changes
As noted earlier, the sodium cation is responsible primarily for maintaining the osmotic integrity of ECV. The signs and symptoms of
hyponatremia and hypernatremia can be detected clinically (Table 4.5),
especially if changes occur rapidly. More commonly, these changes
occur over several days, as noted above. Under such circumstances,
mixed volume and concentration abnormalities often occur. Consequently, it is important that volume status is assessed initially before
any conclusion as to changes in concentration or composition is
ascribed.
Sodium Excess
In surgical patients, this condition is caused primarily by excess
sodium intake (as may occur with infusion of isotonic saline) and
renal retention. The proximal signal for these events is a stress response
to injury or operation. Chronic sodium excess usually results in edema
and weight gain. Classic vascular signs of expanded ECV or frank
heart failure may occur, especially in patients with diseases prone to
causing edema [congestive heart failure (CHF), cirrhosis, nephrotic
syndrome]. Treatment of sodium excess includes eliminating or
reducing sodium intake, mobilization of edema fluid for renal excretion (such as osmotic diuretics for fluid and solute diuretics for
sodium), and treatment of any underlying disease that enhances
sodium retention. An algorithm for assessment of fluid status and
acute sodium changes is shown in Algorithm 4.1.
Sodium Deficit
In the surgical patient, this condition usually occurs via loss of
sodium without adequate saline replacement. Several additional
sources of sodium loss should be considered, including gastrointestinal fluids and skin. Third-space losses of sodium (and water) also can
be extensive after major injury or operation. The symptoms and signs
of sodium deficit arise from hypovolemia and reduced tissue perfusion. Under such circumstances, urine sodium is low (<15 mEq/L) and
osmolarity is increased (>450 mOsm/L). Prerenal azotemia may be
evident (serum BUN/creatinine ratio >20 : 1). Loss of skin turgor also
may occur. Treatment of sodium deficit is directed toward correction
of the sodium and water contraction of the ECV. If hypotension is
present, this must be treated with normal saline or lactated Ringer’s
Salivation, lacrimation, watery diarrhea
“Fingerprinting” of skin (sign of intracellular
volume excess)
Oliguria that progresses to anuria
None
Tissue
Renal
Metabolic
Hypernatremia (water deficit)
Moderate:
Severe:
Restlessness
Delirium
Weakness
Maniacal behavior
Source: Reprinted from Shires GT, Shires GT III, Lowry S. Fluid, electrolyte and nutritional management of the surgical patient. In: Schwartz SI, ed. Principles of Surgery,
6th ed. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies.
Fever
Oliguria
Decreased saliva and tears
Dry and sticky mucous membranes
Red, swollen tongue
Flushed skin
Changes in blood pressure and pulse secondary Tachycardia
to increased intracranial pressure
Hypotension (if severe)
Severe:
Convulsions
Loss of reflexes
Increased intracranial pressure
(decompensated phase)
Cardiovascular
Type of sign
Hyponatremia (water intoxication)
Central nervous Moderate:
system
Muscle twitching
Hyperactive tendon reflexes
Increased intracranial pressure (compensated
phase)
Table 4.5. Consequences of abnormal sodium concentration.
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
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S.F. Lowry
Table 4.6. Composition of parenteral fluids (Electrolyte Content,
mEq/L).
Solutions
Extracellular fluid
Ringer’s lactate
0.9% sodium chloride
D5 45% sodium
chloride
D5 W
M/6 sodium lactate
3% sodium chloride
Na
142
130
154
77
Cations
K
Ca
4
5
4
3
—
—
—
—
Mg
3
—
—
—
Cl
103
109
154
77
—
167
513
—
—
—
—
—
—
—
—
513
—
-1
—
Anions
Osmolality
HCO3
(mOsm)
27
280–310
28*
273
—
308
—
407
—
167*
—
253
334
1026
Source: Reprinted from Borzotta AP. Nutritional support. In: Polk HC Jr, Gardner B,
Stone HH, eds. Basic Surgery, 5th ed. St. Louis: Quality Medical Publishing Inc., 1995.
solution. A mild sodium deficit without symptoms may be treated over
several days if the losses of sodium have been reduced.
Administration of fluids for water and sodium requires knowledge
of the current fluid and electrolyte status of the patient, understanding
of the level of stress, and appreciation for actual or potential sources of
ongoing fluid and electrolyte losses. Having estimated the fluid and
sodium status of the patient, administration of appropriate volumes of
water and sodium usually is done by the intravenous route. Standard
solutions of known contents nearly always are used, and the prescribing physician must be familiar with these basic formulas (Table 4.6).
Abnormalities of other electrolytes (K, Ca, P, Mg: see Abnormalities of
Electrolytes, below) usually require specific fluid solutions or addition
of these ions to standard solutions. Changes in acid–base balance also
may require special alkalotic or acidotic solutions to correct these
abnormalities (Tables 4.7 and 4.8).
Table 4.7. Alkalinizing solutions.*
Solution
NaHCO3
NaHCO3
NaHCO3
Na lactate
1/6 molar
NaHCO3
Tonicity
Isotonic
Hypertonic
Hypertonic
Isotonic
%Solution
1.5
7.5
8.3
1.9
Volume
1L
50 mL
50 mL
1L
Electrolytes
total mEq
Na
HCO3
180
180
45
45
50
50
167
167
Hypertonic
5.0
500 mL
300
300
* Some IV alkalinizing solutions are provided with their tonicity, concentration, volume,
and mEq of Na and HCO3. The liver converts each mEq of Na lactate of 1 mEq of NaHCO3.
3.75 g of NaHCO3 contains 45 mEq of NA and 45 mEq of HCO3. Solution 1 is made by
taking 800 mL of 5% D/W and adding four ampules of 50 mL (200 mL) of 7.5% NaHCO3.
Also, one or more 50-mL ampules of 7.5 NaHCO3 (No. 2) can be added to
l L of 5% D/W or 1/2 N saline and will provide 1 amp. = 45, 2 amps. = 90, and 3 amps. =
135 mEq of Na and HCO3 to the IV solution.
Source: Reprinted from Pemberton LB, Pemberton DK. Treatment of Water, Electrolyte,
and Acid-Base Disorders in the Surgical Patient. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies.
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
TABLE 4.8. Acidifying solutions.*
Solution
NH4 C1
NH4 C1
HC1
Tonicity
Hypertonic
Hypertonic
Isotonic
Percent
Volume
26.75
2.14
0.1 N
20 mL
1L
1L
Electrolytes
total mEq
NH4
C1
100
400
100
100
400
100
* Acidifying solutions that can be used to treat metabolic alkalosis. These solutions
would be used only if KC1 and NaC1 IV solutions were unable to correct the alkalosis.
Source: Reprinted from Pemberton LB, Pemberton DK. Treatment of Water, Electrolyte,
and Acid-Base Disorders in the Surgical Patient. New York: McGraw-Hill, 1994. With
permission of The McGraw-Hill Companies.
Disorders of Composition
By definition, composition changes include alterations in acid–base
balance plus changes in concentration of potassium, calcium, magnesium, and phosphate.
Acid–Base Balance
There are four major buffers in the body: proteins, hemoglobin, phosphate, and bicarbonate. All serve to maintain the hydrogen ion concentration within a physiologic range. Bicarbonate is by far the largest
of these buffer pools and follows the equation:
H+ + HCO3 ´ H2CO3 ´ H2O + CO2
This buffer system involves regulation of CO2 by the lungs and HCO3
by the kidneys. Changes in CO2 are reflected as Paco2 in arterial blood
gases. Respiratory acid–base abnormalities are identified readily by
determination of Paco2. By contrast, there are no definitive means to
identify a “metabolic” acid–base abnormality. Two approaches have
been used. The first is the concept of anion gap, which is used to identify a nonvolatile or fixed acid–base abnormality. Given that many
blood anions are not measured routinely, the difference between the
measured cations and anions is called the “anion gap” [Anion gap =
Na - (HCO3 + Cl)]. The normal value is 12. Metabolic acidosis is the
most common reason for increases with accumulation of anions such
as lactate, acetoacetate, sulfates, and phosphates. (Note: hyperchloremic acidosis may occur without an anion gap.)
The second approach involves measurements of base excess and base
deficit. Base excess measures the amount of nonvolatile acid loss or
extra base that has increased the total buffer base. Base deficit measures the amount of lost base or extra acid that has decreased the buffer
base. The normal value is 0 ± 2.5 mEq/L. Base excess (>2.5 mEq/L) represents metabolic alkalosis, whereas base deficit (<-2.5 mEq/L) represents metabolic acidosis. The four types of acid–base abnormalities are
shown in Table 4.9.
• Respiratory acidosis results from hypoventilation with retention of
CO2. This frequently occurs in postoperative patients who have
received heavy sedation or have been extubated prematurely.
75
Excessive loss of CO2
(increased alveolar
ventilation)
Retention of fixed
acids or loss of base
bicarbonate
Loss of fixed acids
Gain of base
bicarbonate
Potassium depletion
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
≠ Numerator
ratio >20 : 1
Ø Numerator
ratio <20 : 1
Ø Denominator
ratio >20 : 1
Hyperventilation:
Emotional distress,
severe pain, assisted
ventilation, encephalitis
Diabetes, azotemia,
lactic acid accumulation,
starvation
Diarrhea, small bowel
fistulas
Vomiting or gastric
suction with pyloric
obstruction
Excessive intake of
bicarbonate
Diuretics
≠ Denominator
ratio <20 : 1
BHCO3 20
=
H 2CO3
1
Depression of respiratory
center: morphine, CNS
injury
Common causes
Renal
Retention of bicarbonate
Excretion of acid salts,
increased ammonia
formation
Chloride shift into red cells
Renal
Excretion of bicarbonate,
retention of acid salts,
decreased ammonia
formation
Pulmonary (rapid)
Increased rate and depth
of breathing
Renal (slow) as in
respiratory acidosis
Pulmonary (rapid)
Increased rate and depth of
breathing
Renal (slow) as in
respiratory alkalosis
Compensation
CNS, central nervous system.
Source: Reprinted from Shires GT, Shires GT III, Lowry S. Fluid, electrolyte and nutritional management of the surgical patient. In: Schwartz SI, ed. Principles of Surgery,
6th ed. New York: McGraw-Hill, 1994. With permission of The McGraw-Hill Companies.
Retention of CO2
(decreased alveolar
ventilation)
Defect
Respiratory acidosis
Type of acid–base
disorder
Table 4.9. Commonly encountered acid-base disorders.
76
S.F. Lowry
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
77
• Respiratory alkalosis results from hyperventilation leading to
depressed arterial levels of CO2. It may occur in patients experiencing pain or those undergoing excessive mechanical ventilation. Alkalosis causes a shift in the oxyhemoglobin-dissociation curve that can
lead to tissue hypoxia. Respiratory alkalosis also can lead to reduced
levels of potassium and calcium.
• Metabolic acidosis results from the overproduction of acid (lactate,
ketoacidosis) and also may result from excessive loss of bicarbonate
from diarrhea or bowel fistulas.
• Metabolic alkalosis is caused by loss of fixed acid or bicarbonate
retention. As discussed in Case 2, a classic example is loss of acidrich gastric juice via nasogastric tubes. Usually, there is an associated
ECV depletion. Total body potassium and magnesium deficits
mandate judicious replacement. Occasionally, 0.1 N hydrochloric
acid infusions are needed to reverse the alkalosis.
Regardless of whether the initial acid–base disorder is metabolic
or respiratory, a secondary compensatory response occurs within the
other system. The changes associated with acute and compensated
acid–base disorders are shown in Table 4.10. This opposes the pH
abnormality and seeks to restore balance. The adequacy of that compensatory response may be impaired by a variety of associated conditions or medications. If the pH value is in the same direction as the
respiratory diagnosis (low pH and elevated Paco2), then the respiratory problem is primary. Opposing changes in pH and Paco2 suggest
a primary metabolic diagnosis.
Abnormalities of Electrolytes
Potassium: Only about 2% of total body potassium is located in the
ECV. Nevertheless, slight alterations in plasma potassium may dramatically alter muscle and nerve function. As a consequence, abnormalities of potassium concentration require expeditious treatment.
Table 4.10. Respiratory and metabolic components of acid–base disorders.
Type of acid–base
disorder
pH
Respiratory acidosis
Respiratory alkalosis
Metabolic acidosis
Metabolic alkalosis
ØØ
≠≠
ØØ
≠≠
Acute (Uncompensated)
Plasma
PCO2
HCO3-*
(respiratory
(metabolic
component)
component)
≠≠
ØØ
N
N
N
N
ØØ
≠≠
Chronic (partially compensated)
Plasma
PCO2
HCO3-*
(respiratory
(metabolic
pH
component)
component)
Ø
≠
Ø
≠
≠≠
ØØ
Ø
≠?
≠
Ø
Ø
≠
* Measured as levels of standard bicarbonate, whole blood buffer base, CO2 content, or CO2 combining power. The
base excess value is positive when the standard bicarbonate level is above normal and negative when the standard
bicarbonate level is below normal.
Source: Reprinted from Shires GT, Shires GT III, Lowry S. Fluid, electrolyte and nutritional management of the surgical patient. In: Schwartz SI, ed. Principles of Surgery, 6th ed. New York: McGraw-Hill, 1994. With permission of
The McGraw-Hill Companies.
78
S.F. Lowry
Hyperkalemia (>6 mEq/L) requires immediate intervention to
prevent refractory cardiac arrhythmias. Sudden increases in potassium
level usually are caused by infusion or increased transcellular flux
resulting from tissue injury or acidosis. More chronic elevations of
potassium suggest an impairment of renal excretion. Algorithm 4.2
addresses treatment of hyperkalemia.
Hypokalemia in the surgical patient usually results from unreplaced
losses of gastrointestinal fluids (diarrhea, massive emesis) (see Table
4.2 for composition of gastrointestinal fluids). Hypokalemia also may
exist or be exaggerated by renal tubular disorders, diuretic use, metabolic alkalosis, some medications, and hormonal disorders (primary
aldosteronism, Cushing’s syndrome). The treatment of hypokalemia
is directed toward rapid restoration of extracellular potassium concentration followed by slower replenishment of total body deficits.
This approach would be appropriate for Case 2. This can be accomplished by infusion of 20 to 40 mEq of potassium/hour and must be
accompanied by continuous electrocardiogram (ECG) monitoring at
higher rates. Restoration of other abnormalities, such as alkalosis, also
should be addressed.
Calcium: Nearly 99% of body calcium is located in bone. Calcium
located in body fluid circulates as free (40%) or bound to albumin (50%)
or other anions. Only the free component is biologically active.
Acid–base abnormalities alter the binding of calcium to albumin.
(Alkalosis leads to a reduction in ionized calcium, whereas acidosis
increases ionized calcium levels.) Most of the ingested calcium is
excreted in stool. Replacement of calcium usually is not necessary
for routine, uncomplicated surgical patients. However, attention to
replacement may be required in patients with large fluid shifts, immobilization, and especially in patients with surgical thyroid or parathyroid disorders.
Hypercalcemia most often results from hyperparathyroidism and
malignancy. Symptoms of hypercalcemia may include confusion,
lethargy, weakness, anorexia, vomiting, constipation, and pancreatitis.
Nephrogenic diabetes insipidus also may result. Serum calcium
concentrations above 14 mg/dL or any level associated with ECG
abnormalities requires urgent treatment. Virtually all such patients,
such as the one described in Case 3, are dehydrated and require hydration with saline. Additional treatments may include diuretics as well
as diphosphanates, calcitonin, or mithramycin. Steroids may be useful
in some patients.
Hypocalcemia results from several mechanisms, including low
parathormone activity, low vitamin D activity, and conditions referred
to as pseudohypocalcemia (low albumin, hyperventilation). Acute conditions such as pancreatitis, massive soft tissue infections, high-output
gastrointestinal fistulas, and massive transfusion of citrated blood also
may lead to acute hypocalcemia. The early symptoms of hypocalcemia
include numbness or tingling of the circumoral region or fingertips.
Tetany and seizure may occur at very low calcium levels. Replacement
of calcium requires an appreciation of the causes and symptoms. For
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
79
Patient is hyperkalemic
Assess immediate risk. Evaluate renal function.
Monitor ECG continuously.
Kidneys are functioning
Patient is in renal failure
Initiate dialysis.
Serum potassium < 6.0 mEg/L; no
ECG changes are present
Serum potasslum > 6.0 mEq/L, or
ECG changes are present
Administer cation exchange resins. Give
orally if tolerated. If not, give rectally.
Administer cation exchange resins. Give
orally if tolerated. If not, give rectally.
Patient is not receiving
digitalis
Patient is receiving
digitalis
Give 10% calcium gluconate,
10 ml I.V. over 2 min.
If ECG changes persist,
repeat over 15 min.
Give sodium bicarbonate,
45 mEq I.V. over 5 min.
ECG changes resolve
ECG changes persist
Give sodium bicarbonate, 45 mEq I.V. over 5 min.
If ECG changes persist, repeat over 15 min.
ECG changes resolve
ECG changes persist
Give 1 ampule D50W with 10 U regular insulin
I.V. over 15 min. If patient is well hydrated,
consider furosemide, 20–40 mg I.V.
ECG changes resolve
ECG changes persist
Initiate dialysis.
Algorithm 4.2. Assessment and treatment of hyperkalemia. (Reprinted from Van Zee KJ, Lowry SF.
Life-threatening electrolyte abnormalities. In: Wilmore DW, Cheung LY, Harken AH, et al, eds. ACS
Surgery: Principles and Practice (Section 1: Resuscitation). New York: WebMD Corporation, 1997, with
permission.)
80
S.F. Lowry
acute symptomatic patients, intravenous replacement may be
necessary.
Magnesium: Approximately 50% of body magnesium is located in bone
and is not readily exchangeable. Like potassium, magnesium is an
intracellular cation that tends to become depleted during alkalotic conditions. Magnesium absorption occurs in the small intestine, and the
normal dietary intake approximates 20 mEq/day.
Hypomagnesemia may occur secondary to malabsorption, diarrhea,
hypoparathyroidism, pancreatitis, intestinal fistulas, cirrhosis, and
hypoaldosteronism. It also may occur during periods of refeeding after
catabolism or starvation. Low magnesium levels also often accompany
hypocalcemic states, and the symptoms of deficiency are similar. Often,
repletion of both ions is necessary to restore normal function. Up to
2 mEg/kg daily may be administered in the presence of normal
renal function. Attention to restoration of any fluid deficits also is
mandatory.
Hypermagnesemia most frequently occurs in the presence of renal
failure. Acidosis exacerbates this condition. Use of magnesiumcontaining antacids also may lead to elevated serum levels. Emergency
treatment of symptomatic hypermagnesemia requires calcium salts,
and definitive treatment may require hydration and renal dialysis.
Phosphate: Phosphate is the most abundant intracellular anion,
whereas only 0.1% of body phosphate is in the circulation. Consequently, blood levels do not reflect total body stores.
Hypophosphatemia may result from reduced intestinal absorption,
increased renal excretion, hyperparathyroidism, massive liver resection, or inadequate repletion during recovery from starvation or
catabolism. Tissue oxygen delivery may be impaired due to reduced
2,3-diphosphoglycerate levels. Muscle weakness and malaise accompany total body depletion. Prolonged supplementation may be
necessary in severely depleted patients.
Hyperphosphatemia often occurs in the presence of impaired renal
function and may be associated with hypocalcemia. Hypoparathyroidism also reduces renal phosphate excretion.
Summary
Abnormalities of fluid balance, electrolyte imbalance, and acid–
base status are very common in surgical patients. While one must
address acute, life-threatening abnormalities expeditiously, a systematic approach to evaluating each patient should be a routine component
of surgical care. Addressing fluid, electrolyte, and acid–base status is
part of the care plan for every patient. The surgeon should anticipate clinical conditions that can present with or eventuate in such
abnormalities.
4. Fluid, Electrolyte, and Acid–Base Disorders in the Surgery Patient
Selected Readings
Goldborger E. Primer of Water, Electrolyte and Acid–Base Syndromes, 7th ed.
Philadelphia: Lea & Febiger, 1986.
Nathens AB, Maier RV. In: Norton JA, Bollinger RR, Chang AE. et al, eds.
Surgery: Basic Science and Clinical Evidence. New York: Springer-Verlag,
2001.
Pemberton LB, Pemberton PG. Treatment of Water, Electrolyte, and Acid–Base
Disorders in the Surgical Patient. New York: McGraw-Hill, 1994.
Polk HC, Gardner B, Stone HH. Basic Surgery, 5th ed. St. Louis: Quality
Medical Publishing, 1995.
Shires GT, Shires GT III, Lowry S. Fluid electrolyte and nutritional management of the surgical patient. In: Schwartz SI, ed. Principles of Surgery, 6th
ed. New York: McGraw-Hill, 1994.
81