2

F L U I D S ,
E L E C T R O L Y T E S ,
A C I D - B A S E

A N D

B A L A N C E

FRED S. BONGARD

fficient management of fluid and electrolye disorders

is an important part of the daily care of inpatients. Unfortunately, the lengthy and esoteric lectures in many books
and on rounds make the subject confusing for students.
This chapter discusses this vital topic by illustrating the
care of two patients and reviews the physiology and mechanics of order writing in fluid and electrolyte/acid-base
management.

CASE 1
GASTRIC OUTLET OBSTRUCTION
A 55-year-old male had a long history of peptic ulcer disease. Despite multiple attempts at medical management,
he continued to experience epigastric pain and vomiting.
On presentation to the emergency room, his abdomen
was distended with increased dullness to percussion over
the epigastrium. He appeared mildly dehydrated but was
not hypotensive and had no orthostatic blood pressure
changes. An NG tube returned 1,000 ml of nonbilious
material. He was admitted to the hospital and started on
an IV infusion of D5W at 150 ml/hr (he weighed 70 kg)
with no oral intake.
Over the next several days, the NG tube continued to
produce 50 ml/hr of clear nonbilious aspirate. After several days, he began to complain of weakness, generalized
fatigue, and constipation. A chemistry panel showed a
potassium of 2.8 mEq/L, chloride of 84 mEq/L, and bicarbonate of 31 mEq/L. Potassium replacement was
begun with 40 mEq KCl over 6 hours. A repeat electrolyte panel the next day detected a potassium concentra-

tion of 3.0 mEq/L. Blood gas analysis showed a pH of 7.52

and a bicarbonate concentration of 32 mEq/L.

CASE 2
POSTOPERATIVE COMPLICATION
A 52-year-old woman (50 kg) was admitted for elective
sigmoid colectomy for diverticular disease. Her operation went well except for unanticipated blood loss of 1 L
due to inflammation surrounding her left colon. During
the 3-hour operation, she received 5 L of lactated
Ringers solution. The first few days after surgery were
uneventful, with the exception of a continued paralytic
ileus. She was continued on an IV infusion of D5W with
20 mEq KCl/L. On the fifth day, she began to complain
of muscle twitching and anxiety. On the seventh day, she
experienced a generalized seizure. During the postictal
period she was found to be hypertensive, with marked
hyperreflexia. Review of her bedside chart showed that
her urine output had been decreasing over the past several days.
5

C A R E

O F

T H E

S U R G I C A L

P A T I E N T

GENERAL CONSIDERATIONS

ody fluid is found in three spaces: intracellular (42%

of total body weight), interstitial (14%), and intravascular
(7%). Blood fills the intravascular space and is the portion
of the body fluids that clinicians have ready access to.
Skeletal muscle makes up most of the intracellular space
and is the largest collection of fluids and electrolytes. The
interstitial volume is composed of fluid between the other
two compartments. Under pathologic conditions, it fills
with edema fluid and constitutes part of the third space.
Equilibrium between the compartments depends on
the relative concentrations of osmotically active particles
(osmolals [Osm]) in solution. In clinical usage, the term
tonicity is interchangeable with osmolality. The effective
oncotic pressure depends on the number of osmotically
active particles that do not pass freely between the semipermeable membranes that separate the compartments.
In each compartment, the concentration of particles is
normally 285305 mOsm. An increase in the number of
osmolals in one compartment causes a flow of water into
that compartment, decreasing its oncotic pressure.
The effect of volume depletion depends on the composition of the fluid lost (Table 2.1). For example, sweat is extremely hypotonic because it contains very little sodium.
When a high fever is accompanied by severe sweating, the
defect is due primarily to free water loss and results in hypertonic dehydration. This causes fluid to move (translocation) from the interstitial space into the intravascular space,
reducing the increased oncotic pressure. Because body secretions are formed by components in the intravascular
space, fluid loss due to fistulas, diarrhea, and drains ultimately results in intravascular dehydration. The composition of the fluid lost has a profound effect on the patients
fluid and electrolyte balance. For example, gastric secretions are very high in both chloride and potassium (Table
2.1). Thus, gastric suction leaves the intravascular space
low in volume (dehydration), chloride (hypochloremia),
and potassium (hypokalemia). When the loss is from the
gastrointestinal tract, the resulting hypokalemia may be
profound because of the relatively high concentration of
potassium in these fluids (Case 1). In an effort to treat the
electrolyte imbalance, a sample of the drainage or an aspirate should be sent for chemical analysis when the composition is in doubt.

When considering a patients fluid requirements, it is

useful to think about ones own water intake. The average
healthy person consumes about 6 glasses, 812 oz each, for
a total daily intake of 4872 oz (1,4402,160 ml/day). For a
70-kg student, this would be about 2030 ml/kg/day. Therefore, an adult patient without previous deficits (e.g., vomiting, diarrhea, fistulas) and without ongoing losses (nasogastric [NG] tube loss) the basal fluid requirement is 2030
ml/kg. This varies greatly with a number of factors, such as
temperature and the presence of an infection. Smaller patients need less fluid and larger patients need more. A useful rule of thumb for free water requirements is to provide
100 ml/kg/day for the first 10 kg of the patients weight, 50
ml/kg/day for the next 10 kg, and 20 ml/kg/day for each remaining kilogram. A 70-kg patient requires the following:
10 kg 100 ml/kg (1 L) + 10 kg 50 ml/kg (500 ml) + 50 kg
20 ml/kg (1 L) = 2,500 ml/day of free water. A 23-kg child
would need 10 kg 100 ml/kg (1 L) + 10 kg 50 ml/kg (500
ml) + 3 kg 20 ml/kg (60 ml) = 1,560 ml/day of free water.
This formula exceeds the normal intake of most healthy
people, but with normal renal function the excess is well
tolerated and provides a safety net to compensate for increased insensible loss of third spacing seen with fever or
infection. The goal is to maintain adequate intravascular
volume to prevent vital organ ischemia.
Fluid and electrolytes are normally lost through three
routes: (1) urine output, (2) gastrointestinal loss, and (3)
insensible loss. Insensible loss is primarily sweat and respiratory loss that consists primarily of electrolyte free water
(sweat has only 35 mEq Na+/L). This constitutes usually
only 400 ml/m2/day, although fever increases insensible
loss by 10%/C. The loss of free water may produce significant hypertonic dehydration, requiring additional free
water replacement.
Most (80%) ingested water is absorbed between the
distal ileum and the mid-transverse colon. Only 200400
ml of fluid is ultimately lost in the stool. Surgical patients
frequently have increased fluid and electrolyte loss from
the gut. Sources include prolonged gastric suction (Case 1),
intestinal obstruction, fistulas, and diarrhea.
Urine output varies with a number of factors, including activity level, ambient temperature, and fluid intake.
The normal person voids about 45 times per day in volumes of 200250 ml. Following traumatic or surgical
stress, increased secretion of aldosterone in response to

TABLE 2.1 Composition of gastrointestinal secretions

TYPE

OF

SECRETION

VOLUME (ML/24

HR)

NA (MEQ/L)

K (MEQ/L)

CL (MEQ/L)

HCO3 (MEQ/L)

510

2030

515

2530

1015

Saliva

1,0001,500

Stomach

1,0002,000

6090

100130

Pancreas

600800

135145

510

7090

95115

300600

135145

510

90110

3040

2,0003,000

120140

510

90120

3040

Bile
Small intestine

F L U I D S ,

E L E C T R O L Y T E S ,

decreased intravascular pressure causes a physiologic oliguria. Urine excretion may fall as low as 0.51.0 ml/kg/hr.
This commonly occurs during the immediate postoperative period when acceptable urine output is 0.51.0
ml/kg/hr. Under these circumstances, attempts to increase
urine output through the use of diuretics are ill advised
and may worsen dehydration by leading to loss of both
sodium and water. Oliguria is also produced by the action
of antidiuretic hormone (ADH), which is secreted in response to increased serum osmolarity resulting from dehydration. Serum osmolality is estimated using the equation
Serum osmolality (mOsm) = 2 [Na] +

[glucose] [BUN]
+
18
2.8

Normal serum osmolality ranges between 285 and 305

mOsm. Because sodium is the major contributor, increased
sodium produces increased osmolality. The hyperglycemia
that accompanies diabetes or injudicious use of hyperalimentation may also cause hyperosmolarity. Free water
loss causes an increase in the concentration of particles
and stimulates the chemoreceptors in the carotid body.
These in turn relay information to the hypothalamus,
which secretes antidiuretic hormone, promoting the reabsorption of water from the collecting tubules of the kidney
to reduce the bloods osmotic pressure.
Basal requirements for electrolytes must also be considered when writing intravenous fluid orders. Normal requirements are 11.5 mEq/kg/day for sodium, 0.50.75 mEq/kg/
day for potassium, and 11.5 mEq/kg/day for chloride.
Selection of an intravenous fluid and its rate of infusion is not a daunting task. Although a large number of intravenous fluids are available, only the few used regularly
need to be learned (Table 2.2). Most contain a small
amount of dextrose (5%, or 50 g/L), to provide limited
calories (4 kcal/g dextrose = 200 kcal/L), which prevents
protein catabolism.

TABLE 2.2

A N D

A C I D - B A S E

B A L A N C E

Dextrose is also added to some solutions (e.g., D5 12NS)

to make them isosmotic, to avoid red blood cell (RBC)
lysis on infusion. The dextrose quickly crosses cell membranes, where it is used as an energy source, leaving behind only the free water and electrolytes in the intravascular space.
When planning fluid/electrolyte orders, three questions must be answered:
1. What are the patients existing deficits?
2. What is the basal requirement?
3. What are the ongoing losses? Case 1 will serve as an
example.
The 70-kg patient (Case 1) had been vomiting for several days and had 1,000 ml of gastric secretions in his
stomach, when an NG tube was placed. These are pre-existing deficits. The degree of dehydration (loss of free
water) can be estimated using the 2-4-6 rule. The patient
who is mildly dehydrated (e.g., thirsty, decreased urine
output, dry skin, normal blood pressure with minimal orthostatic change) has a fluid deficit of 2% of total body
weight. If the dehydration is more pronounced and includes orthostatic blood pressure changes and decreased
skin turgor, the free water deficit is approximately 4% of
total body weight. When hypotension at rest is present
and oliguria is profound, the deficit is 6% of total body
weight. In the sample case, the patient appears mildly dehydrated, making his estimated pre-existing loss 2% of his
weight, or 1.4 L (1 kg = 1 L). The gastric contents aspirated through the NG tube account for 1.0 L, bringing the
pre-existing deficit to 2.4 L.
The electrolyte composition of the fluid lost is important. The patient had been vomiting gastric contents (presumably he had gastric outlet obstruction from peptic
ulcer disease), which is close to D5 12NS + 20 KCl in composition (Tables 2.1 and 2.2).

Composition of intravenous solutions

GLUCOSE

SOLUTIONS
Extracellular fluid
5% dextrose and water

NA

CL

HCO3

1,000

140

102

27

(G/L)

CA

MG

HPO4

NH4

4.2

0.3

(MEQ/L)

50

100

0.9% sodium chloride (normal saline)

154

154

0.45% sodium chloride (half-normal saline)

77

77

0.21% sodium chloride (14 normal saline)

34

34

3% sodium chloride (hypertonic saline)

513

513

2.7

168

10% dextrose and water

Lactated Ringers solution

130

109

28a

0.9% ammonium chloride

168

aPresent

in solution as lactate, but metabolized to bicarbonate.

C A R E

O F

T H E

S U R G I C A L

P A T I E N T

Replacement of pre-existing loss is best accomplished

over 24 hours, with one-half of the replacement given
over the first 8 hours and the remainder over the ensuing
16 hours. This approach should be modified for older patients with the potential for congestive heart failure who
cannot tolerate large volume infusions. Conversely, in
younger patients who are being prepared for emergency
surgery, the deficit can be replaced quickly. In the sample
patient, the 2.4-L deficit can be repaired with 150 ml/hr of
D5 + 12NS + 20 mg KCl/L over 8 hours (one-half the estimated loss) followed by 75 ml/hr D5 + 12NS over the next
16 hours (the second half of the deficit).
Since patients are often not allowed oral intake, both
fluid and electrolytes must be provided by the parenteral
route. Although formulas can be used to estimate this need,
fluid infusion rates and compositions are guided ultimately
by urine output and blood chemistry determinations.
For the patient described in Case 1, the calculated
maintenance fluid requirement is approximately 2,400
ml/day (100 ml/hr). Since he was not febrile and had no
other reason for increased insensible loss (e.g., mechanical
ventilation with nonhumidifed gas), there was no need to
increase the basal fluid rate. Among the solutions available,
D5W + 12NS + 20 mEq KCl/L will provide the electrolytes
required.
Surgical patients frequently have catheters, fistulas,
and drains, all of which are sources of ongoing fluid and
electrolyte loss. Unless these losses are replaced, dehydration and electrolyte/acid-base imbalances will result. The
volume lost can be measured, while the electrolyte composition can be estimated (Table 2.1). If the source of the
loss (i.e., a fistula) is unknown, a sample of the effluent
should be analyzed for electrolyte composition. Once the
electrolyte content is known, an appropriate replacement
fluid can be selected.
The patient in Case 1 had an NG tube that continued
to produce 50 ml/hr of gastric juice. This can be replaced
on a milliliter to milliliter basis with D5W + 12NS + 20
mEq/L of KCl.
If we combine the three components of pre-existing
loss, basal requirement, and ongoing loss, we find that
fluid therapy over the first 8 hours should consist of D5W
+ 12NS + 20 mEq/L of KCl at 300 ml/hr. For the next 16
hours, it should be reduced to 225 ml/hr. Assuming that
the deficit has been replaced, that the patients urine output is at least 0.51.0 ml/kg/hr, and that the output
through the NG tube remains relatively constant (at 50
ml/hr), the infusion rate should be further reduced to 150
ml/hr at the end of 24 hours. In the problem described in
Case 1, the pre-existing fluid loss, maintenance fluid, and
ongoing loss all use the same electrolyte solution. This is
often not the case, and either a combination of fluids must
be used or a special solution can be prepared by the pharmacy to approximate the patients needs.
As written, the scenario in Case 1 includes only D5W,
with minimal provisions for replacing electrolyte losses

and ongoing requirements. The result was severe dehydration and hyponatremia. Profound derangements of this
type can easily be prevented by remembering the three
components of fluid therapy. Case 2 is reviewed in detail
in Appendix 2.1.

K E Y

P O I N T S

Under pathologic conditions, interstitial space fills with

edema fluid and constitutes part of the third space
Increased number of osmolals in one compartment causes
flow of water into that compartment, decreasing oncotic pressure
Because body secretions are formed by components in the
intravascular space, fluid loss due to fistulas, diarrhea, and
drains ultimately leads to intravascular dehydration
Fluid and electrolytes normally lost through three routes:
urine output, gastrointestinal loss, and insensible loss
Decreased intravascular pressure after traumatic or surgical
stress leads to increased secretion of aldosterone, causing physiologic oliguria; use of diuretics to increase urine output illadvisedmay worsen dehydration, and loss of sodium and water
Most intravenous fluids contain small amount of dextrose
(5%, or 50 g/L), providing limited calories (4 kcal/g dextrose =
200 kcal/L), preventing protein catabolism
Dextrose also added to some solutions (e.g., D5 12 NS making them isosmotic, to avoid RBC lysis on infusion
Replacement of pre-existing loss usually accomplished over
24 hours, with one-half of replacement given over first 8 hours,
and remainder over next 16 hours

FLUIDS AND ELECTROLYTES

odium is the principal extracellular cation (Fig. 2.1)

and the major contributor to extracellular osmolality. The
serum concentration of sodium is not necessarily related
to extracellular volume status, although changes in sodium
concentration usually produce changes in extracellular
fluid volume by shifting free water. Signs and symptoms of
hypo- and hypernatremia usually do not occur unless the
changes are severe or occur rapidly.
Replacement of electrolyte-rich fluid loss with free
water is the most common cause of hyponatremia in surgical patients (Case 2). As the extracellular osmolality falls,
free water shifts into the intracellular space, where it may
cause nervous system symptoms, including increased tendon reflexes, muscle twitching, convulsions, and hypertension (Case 2). Other findings include excessive salivation,
lacrimation, watery diarrhea, and increased intracranial
pressure. The symptoms of hyponatremia depend not only
on its degree, but also on the speed with which it develops. When hyponatremia occurs rapidly, signs and symptoms appear at a concentration as high as 130 mEq/L.
When chronic loss is responsible, findings may not be present until the concentration is as low as 120 mEq/L.

F L U I D S ,

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A N D

A C I D - B A S E

HHCO3

200

HCO3
27

meq/L H2O

150

HCO3 10

Extracellular fluid

175

B A L A N C E

Nonelectrolytes
HHCO3
HCO3
27

125

K+
157

PO43
113

Na+
14

Protein
74

100
Na+
152

75

Cl
113

Na+
143

50

HPO4

25
0

K+ 5
Ca2+ 5
MG2+ 3

Cl
117

1
K+
Ca2+ 5
MG2+ 3

SO4
Org. acid 6

Protein
16

Blood plasma

HPO4

Org. acid 6

Interstitial fluid

SO4 1 Mg
Protein 2

2+

26

Intracellular fluid

FIGURE 2.1 Electrolyte composition of human body fluids. Note that the values are in milliequivalents
per liter (mEq/L) of water, not of body fluid. (From Leaf A, Newburgh LH: Significance of the Body Fluids in Clinical Medicine. 2nd Ed. Thomas, 1955, with permission.)
Sodium deficits should be approximated from the serum
sodium concentration. Because hyponatremia is frequently caused by excess free water administration, the
deficit is often relative rather than real. The sodium deficit
is calculated as follows:
Na deficit = (140 mEq/L measured Na)
(body weight 0.6)
Because sodium distributes throughout total body water,
the quantity (body weight 0.6) is used. Sodium should be
replaced when hyponatremia is profound (<120 mEq/L)
or when the loss occurs rapidly and the patient becomes
symptomatic. No more than one-half the calculated deficit
should be replaced within the first 24 hours. Amyelenosis
may result from excessively enthusiastic replacement.
Normal saline is used, although hypertonic saline (3%
NaCl) may be required in rare circumstances.
Hypernatremia results from the loss of free water in
excess of sodium. It causes weakness, restlessness, and
delirium. The skin becomes dry and the mucous membranes are sticky. Salivation and tear production are decreased, and an increase in body temperature may also
occur. Free water, usually in the form of D5W, is required
and should be administered slowly to prevent a sudden
decrease in osmolarity.
Potassium is the principal intracellular cation (Fig.
2.1). Average oral intake of potassium is 50100 mEq/day,
with the majority excreted in the urine. Large amounts of
potassium are released from injured and burned tissues,
causing hyperkalemia. The symptoms of hyperkalemia are

cardiovascular or gastrointestinal and include nausea,

vomiting, diarrhea, and constipation. Muscle weakness,
loss of deep tendon reflexes, and paralysis occur. Electrocardiographic (ECG) findings include high peaked T
waves (tombstone T waves), widened QRS complexes,
and depressed ST segments. At potassium concentrations
greater than 6 mEq/L, T waves may disappear to be followed by diastolic cardiac arrest.
Hyperkalemia should be treated when concentrations
exceed 5 mEq/L or when signs or symptoms are present.
Management of hyperkalemia revolves primarily around
neutralizing the cardiovascular effect of potassium and
secondarily on decreasing the actual potassium concentration. Calcium antagonizes the actions of potassium and
should be the first drug given. The patient should be given
50100 ml of calcium chloride by rapid intravenous infusion. Reduction of potassium concentration may be accomplished with the intravenous infusion of glucose and
insulin. Potassium enters the cells along with glucose. Although this procedure can rapidly lower the serum potassium, rebound often occurs and potassium levels rise
acutely several hours later. The use of ion exchange resins
such as polystyrene sulfonate (Kayexalate) are helpful. A
slurry of this compound, administered by enema, exchanges sodium for potassium. The exchange resin works
slowly and takes several days of repeat administration
before potassium levels fall into a normal range. All
exogenous sources of potassium should be stopped, and
renal function should be checked to ensure that the patient does not have acute renal failure resulting in potassium retention.

1 0

C A R E

O F

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S U R G I C A L

P A T I E N T

Hypokalemia is more common among surgical patients than is hyperkalemia and usually results from insufficient potassium administration in the face of prolonged
gastrointestinal loss. Because potassium is exchanged for
sodium in the renal tubule, hypovolemia (with production
of aldosterone) exaggerates hypokalemia by increasing
renal loss. Furthermore, because hydrogen and potassium
are in competition for renal reabsorption, alkalosis can
also augment renal excretion. Hypokalemia causes decreased contractility of skeletal, smooth, and cardiac muscle. Signs include paralytic ileus, decreased deep tendon
reflexes, weakness, and ultimately flaccid paralysis. The
ECG exhibits flattening of the T waves, low voltage, depression of ST segments, and appearance of the U wave.
Potassium replacement should be instituted for chemical
(<3.5 mEq/L) or symptomatic hypokalemia. This is particularly important in patients receiving digitalis because hypokalemia sensitizes the myocardium to the effects of digitalis. In patients who cannot take oral supplementation,
intravenous potassium should not be replaced at rates
greater than 1015 mEq/hr. Because potassium is largely
an intracellular ion, relatively small decreases in serum
potassium reflect large whole body potassium deficiencies.
Hence, large quantities of potassium are usually required
over several days for adequate replacement of potassium
deficiencies. In general, a decrease of 1.0 mEq/L in serum
potassium represents a 100200-mEq whole body defect.
When serum potassium is tested shortly after intravenous
infusion, a false sense of security is obtained when the
concentration has risen. However, as the newly administered potassium equilibrates with the intracellular space,
the plasma concentration will drop rapidly. Hence, potassium levels should not be tested until several hours after
infusion has been completed.
The whole body content of calcium is 1,0001,200 g.
Dietary intake is approximately 13 g, with 200 mg excreted in the urine. Serum calcium is largely under the
control of the parathyroid hormone (parathyrine)/calcitonin system. Approximately one-half of the bodys calcium is bound to plasma proteins and is un-ionized. A decrease of 1 g/dl of albumin results in a 0.8 mg/dl decrease
in the measured total serum calcium concentration.
Hence, patients with hypoproteinemia may have a relatively normal calcium concentration in spite of measured
hypocalcemia. Most of the remaining calcium is ionized
and is responsible for neuromuscular conduction and contraction. The extent of calcium ionization is inversely related to pH. As a result, alkalosis worsens hypocalcemia.
The parathyroid glands respond to decreased ionized calcium by secreting parathyrine, which causes increased reabsorption of calcium from the bones, decreased renal excretion of calcium, and increased excretion of phosphate.
The signs and symptoms of hypocalcemia usually appear
at a serum concentration of 8 mEq/L with normal protein
and pH levels. Circumoral paresthesias and tingling in the

fingers and toes along with hyperactive deep tendon reflexes are the first signs. Chevosteks and Trousseaus signs,
carpopedal spasm, tetany, and convulsions occur with further decreases. The ECG shows prolongation of the QT
interval.
Acute hypocalcemia should be treated with an intravenous infusion of either calcium gluconate or calcium
chloride. Calcium gluconate contains 93 mg of Ca2+ in 10
ml, while calcium chloride contains 273 mg of Ca2+ in 10
ml, making calcium chloride the agent of choice. Hypocalcemia may be produced by massive blood transfusions because the citrate preservative in the banked blood chelates
calcium. In this case, calcium should be replaced at a dose
of 0.2 g of calcium for every 500 ml of blood transfused. A
common misconception is that calcium supplementation
is required after transfusion for normal hemostasis; however, blood will clot normally with very small calcium concentrations. The supplementation requirement stems
from the need for cardiac contractility and excitation-contraction coupling.
Hypercalcemia among surgical patients may stem
from hyperparathyroidism, injudicious calcium administration, the milk-alkali syndrome, or the paraneoplastic
syndrome. Many tumors are endocrinologically active and
produce hormone-like substances such as parathyrine.
Symptoms of hypercalcemia include weakness, nausea,
vomiting, abdominal complaints, and anorexia. Other findings include back and extremity pain, thirst, polydypsia,
polyuria, stupor, and coma. When calcium levels reach 16
mEq/L, immediate treatment should be instituted. The
initial management of hypercalcemic crisis is the induction of a saline diuresis. Furosemide causes renal excretion of calcium and lowers the calcium level. Sufficient
volumes of saline are required to ensure diuresis and prevent hypovolemia. Other methods to reduce the calcium
concentration include phosphate supplementation and the
use of corticosteroids and mithramycin. Phosphate supplementation binds calcium and reduces bone reabsorption. It produces metastatic calcium phosphate deposits,
which may be deleterious when they form in organs such
as the eye or kidney. Corticosteroids decrease the reabsorption of calcium from bone and the intestinal tract and
are useful in select patients with systemic diseases such as
sarcoidosis, leukemia, or lymphoma. Mithramycin is an
antineoplastic drug that decreases osteoclastic activity. Because it may take weeks to act and has several undesirable
side effects, it is seldom used.
More than one-half of the bodys 2,000-mEq content
of magnesium is complexed in bone; the remainder is
within the cells. The normal plasma magnesium concentration is 1.52.5 mEq/L, constituting a balance between
the daily dietary intake of 250 mEq/day and loss in stool.
Most body fluids, including many secretions, have a magnesium content of 23 mEq/L. Magnesium activates cholinesterase and therefore plays a crucial role in controlling

F L U I D S ,

E L E C T R O L Y T E S ,

striated muscle activity. Deficits of magnesium lead to uncontrolled myoneural conduction and excessive muscular
activity. Magnesium is also an integral part of the phosphorylating enzymes used in carbohydrate metabolism.
Hypomagnesemia is common among alcoholics, with gastrointestinal malabsorption syndromes, with chronic diarrhea, after prolonged use of loop diuretics such as
furosemide or ethacrynic acid, with pancreatitis or gastrointestinal fistula, and with hypoparathyroidism. Hypomagnesemia produces gross tremors, hyperreflexia, muscle fibrillation, transitory hallucinations, arrhythmias, and
Chvosteks and Trousseaus signs (hypomagnesemic
tetany). Hypomagnesemia is treated with oral or intravenous magnesium, the latter in the form of magnesium
sulfate. Renal function should be assessed before magnesium replacement is given because magnesium accumulates in renal failure. Because 80% of administered magnesium is excreted in the urine, a significant amount must
be given to correct even a small deficit. This is best done
(in a patient with normal renal function) by giving 20 ml of
20% MgSO4 as an intravenous bolus, followed by 500 ml
of 20% MgSO4 every 6 hours (qid) until the concentration
normalizes (1 g of magnesium contains 8 mEq of Mg2+).
When large doses of magnesium are given, the ECG
should be monitored for signs of toxicity (similar to those
seen with hyperkalemia) to avert cardiac arrest.
Hypermagnesemia (prolonged levels over 56 mEq/L)
result in arrhythmia, lethargy, hyporeflexia, and weakness.
This occurs most commonly in patients with renal failure
or when excessive magnesium replacement has been administered over a long period. Rapid increases in magnesium concentration should be treated by infusion of calcium chloride or calcium gluconate. Hypermagnesemia
due to renal failure is best treated by hemodialysis.
Hypophosphatemia is the most common disturbance related to phosphate and is usually secondary to decreased intake among patients receiving total parenteral nutrition
(TPN). It may also occur among cirrhotics and in those with
either hypo- or hyperparathyroidism. Mild deficits (<3.0
mEq/dl) result in hyperglycemia because intracellular phosphorylation of glucose is required after glucose enters the
cell. Hypophosphatemia allows glucose to leak from cells.
Moderate nutrition-related deficits occur among alcoholics
(<2.0 mEq/dl) and present as weakness, malaise, and
chronic debility. Severe deficits (<1.0 mEq/dl) cause decreased energy stores by affecting mitochondrial adenosine
triphosphate (ATP) production and by limiting oxygen unloading to the tissue by reducing 2,3-diphosphogluconate
(2,3-DPG) concentrations. Hypophosphatemia is treated by
administration of either sodium or potassium biphosphate.
The patient is given either 12 mg/kg PO or isotonic
buffered sodium phosphate (200500 ml tid IV). If phosphate is administered too quickly, it will complex with calcium and produce hypocalcemia, which can lead to hypotension and renal failure.

A N D

K E Y

A C I D - B A S E

B A L A N C E

1 1

P O I N T S

Sodium
Concentration not necessarily related to extracellular volume
status, although changes in sodium concentration usually produce changes in extracellular fluid volume by shifting free
water
Replacement of electrolyte-rich fluid loss with free water
most common cause of hyponatremia in surgical patients;
symptoms depend not only on degree, but also on speed of
development
Potassium
Potassium is principal intracellular cation
Symptoms of hyperkalemia are cardiovascular or gastrointestinal (nausea, vomiting, diarrhea, and constipation)
Hyperkalemia should be treated when concentrations exceed
5 mEq/L or when signs or symptoms present
Calcium antagonizes actions of potassium; should be first
drug given
Hyperkalemia more common among surgical patients; usually results from insufficient potassium administration during
prolonged gastrointestinal loss
Signs include paralytic ileus, decreased deep tendon reflexes,
weakness, ultimately flaccid paralysis
Potassium replacement necessary for chemical (<3.5 mEq/L)
or symptomatic hypokalemia, particularly in patients on digitalis, because myocardium sensitized to its effects
Decreases of 1.0 mEq/L in serum potassium generally represents a 100200-mEq whole body deficit
Calcium
Decrease of 1 g/dl albumin results in 0.8-mg/dl decrease in
measured total serum calcium concentration
Signs and symptoms of hypocalcemia usually appear at
serum concentration of 8 mEq/L with normal protein and pH
levels; first signs are circumoral paresthesias and tingling in fingers and toes, along with hyperactive deep tendon reflexes
Acute hypocalcemia treated with intravenous infusion of calcium gluconate or calcium chloride
Symptoms of hypercalcemia include weakness, nausea, vomiting, abdominal complaints, and anorexia
Initial management of hypercalcemic crisis is induction of
saline diuresis
Magnesium
Most body fluids have magnesium content of 23 mEq/L
Magnesium activates cholinesterase and therefore plays crucial role in controlling striated muscle activity
Hypomagnesemia produces gross tremors, hyperreflexia,
muscle fibrillation, transitory hallucinations, arrhythmias, and
Chvosteks and Trousseaus signs
Hypomagnesemia treated with oral or intravenous magnesium sulfate; with large doses, monitor ECG for toxicity, as in
hyperkalemia, to avert cardiac arrest

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Hypermagnesemia (prolonged levels >56 mEq/L) result in

arrhythmia, lethargy, hyporeflexia, and weakness
Phosphate
Hypophosphatemia usually secondary to decreased intake
among patients receiving total parenteral nutrition

ACID-BASE BALANCE

cid-base balance depends on the relative concentration of hydrogen ion and its buffer systems. In general, any
decrease in bicarbonate (or increase in protons) will result
in acidosis, while any increase in bicarbonate (or decrease
in protons) will result in alkalosis. Recall that hydrogen ions,
bicarbonate, and carbon dioxide are in equilibrium:
H+ + HCO3 H2CO3 H2O + CO2
The increase in proton concentration may occur as a result
of the addition of an acid (most metabolic processes produce weak acids) or by an increase in the concentration of
carbon dioxide (respiratory failure). Physiologic acids are
either volatile or fixed. Fixed acids are those that can only
be excreted by the kidneys, while volatile acids (carbon
dioxide) are removed by the lungs. A drop in pH because
of an increase in fixed acids is termed metabolic acidosis;
when caused by carbon dioxide accumulation, respiratory
acidosis has occurred. Decreased hydrogen concentration
(increased pH) produces metabolic or respiratory alkalosis.
Changes in the concentration of hydrogen ions are
buffered by several systems, including the bicarbonate
buffer, protein buffers, and the hemoglobin buffering system. Although changes in the bicarbonate system are the
principal early defenses, the protein buffering system is
much larger and can absorb greater concentrations of acid
than can the bicarbonate system.
The respiratory system responds quickly to the accumulation of metabolic acids. As protons accumulate, they
are buffered by the bicarbonate system, producing carbon
dioxide and water. An increase of 10 mmHg of carbon
dioxide causes a decrease in pH of 0.08. The altered pH
stimulates the aortic chemoreceptors, which in turn stimulate the respiratory center to increase the rate and volume
of breathing. Such Kussmaul ventilation eliminates carbon
dioxide from the blood. This respiratory compensation for
metabolic acidosis occurs quickly but is somewhat limited
in its ability to offset a large accumulation of acid. Contrary
to popular belief, pulmonary retention of carbon dioxide
(so-called compensatory respiratory acidosis) does not
occur significantly in response to metabolic alkalosis.
The kidney has the greatest capacity to correct disturbances in acid-base balance. It protects against both acidosis and alkalosis by excreting acid during acidosis and al-

kali during alkalosis. Renal acidification can lower urine

pH to as low as 4.5. This mechanism is so important to
homeostasis that virtually all forms of renal insufficiency
ultimately result in metabolic acidosis because of the impaired ability to secrete acids.
Common causes of metabolic acidosis among surgical
patients include cellular ischemia (hypoxia), diabetic acidosis, ketosis, rhabdomyolysis, and major trauma. Cellular
hypoxia, due to shock, cardiac arrest, hypothermia, or
heart failure, leads to decreased oxygen delivery for the
aerobic metabolism of glucose. This causes lactate to accumulate, producing lactic acidosis. Although relatively
uncommon in surgical practice, ingestion of salicylates,
paraldehyde, methanol, or acetazolamide (carbonic anhydrase inhibitor) also causes metabolic acidosis. The symptoms of metabolic acidosis include Kussmaul respiration,
decreased cardiac output, disorientation, lethargy, and dehydration. When the acidosis is mild (pH >7.2) a rightward shift in the oxyhemoglobin dissociation curve partially compensates for the decreased cardiac output by
increasing the unloading of oxygen to the tissues.
To aid in determining the cause of a metabolic acidosis, clinicians frequently divide acidosis into two groups:
those with an anion gap and those without. The anion gap
is calculated as follows:
Anion gap = 2 [Na+] ([HCO3] + [Cl ])
Because the number of anions and cations must be
equal in order to preserve electroneutrality, the total number of cations must equal the total number of measured
and unmeasured anions. Sodium represents the vast majority of the cations in the extracellular space, while bicarbonate and chloride together constitute most of the anions. However, there is normally a small deficit when the
anion concentration is subtracted from the cation concentration. This gap is composed of anions not normally
measured in routine laboratory determinations. These anions are usually the salts of weak acids, such as lactate,
pyruvate, malate, citrate, amino acids, sulfates, and free
fatty acids. Under normal conditions, the anion gap is less
than 14 mEq/L. Any decrease in the bicarbonate concentration or increase in the number of weak acid salts, or
both, will widen the gap and produce an anion gap acidosis. Common causes of high gap acidosis include diabetic
ketoacidosis, uremia, aspirin ingestion, lactic acidosis, and
infection. Although nongap acidosis can occur (from the
addition of chloride), it is far less common.
The guiding principle in the treatment of metabolic
acidosis (high gap or otherwise) is to identify and correct
the underlying process. This may require repair of hypovolemia, drainage of an infection, or improvement of myocardial contractility with the use of an inotropic agent
such as dopamine. As this is being done, pharmacologic
correction with base may be required if the acidosis has

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become severe. Sodium bicarbonate is the agent of choice.

However, sodium bicarbonate must be used with extreme
caution when the patient has an associated respiratory acidosis because neutralization of the excess protons will result in the production of carbon dioxide, which must be
excreted by the lungs.
The amount of bicarbonate required can be determined when the base deficit is known. The base deficit is
calculated during the automated measurement of blood
gases. It represents that portion of the acidosis (or alkalosis) that is due to a metabolic component. Hence, if the
pH is 7.2 and the arterial partial pressure of carbon dioxide (PaCO2) is normal (40 mmHg), the acidosis must be of
metabolic origin, exclusively, and the base deficit will be
elevated (normal = 2). On the contrary, if the pH is 7.32
and the PaCO2 is 50, the acidosis is purely of respiratory
origin, and the base deficit will be 0. The amount of base
required to achieve full correction of the metabolic component of an acidosis is calculated as follows:
mEq base required = 0.4 base deficit body weight (kg)
The term 0.4 is used because virtually all of the disturbance occurs in the extracellular space, which is approximately 40% of the total body weight. Hence, if a 70-kg patient with a pH of 7.1 has a base deficit of 15, the required
amount of base would be: 15 (0.4 70), or 420 mEq
HCO3. Since each ampule of sodium bicarbonate contains 44.6 mEq of base, approximately 912 ampules of bicarbonate would be needed to reverse the metabolic acidosis completely. Profound disturbances should not be
corrected rapidly. Approximately one-half of the calculated requirement should be administered over 8 hours,
with the rest given over the ensuing 16 hours. Rapid infusions of bicarbonate can produce profound respiratory acidosis if any element of respiratory failure is present in a
spontaneously breathing patient.
Metabolic alkalosis occurs relatively infrequently among
surgical patients; however, it may be life-threatening when
severe. It consists of the triad of (1) increased pH, (2) increased HCO3, and (3) decreased serum chloride concentration. Because the decline in chloride does not compensate for the rise in bicarbonate, the anion gap
increases. Metabolic alkalosis is produced by vomiting,
prolonged gastric suction, use of diuretics, and volume depletion (contraction alkalosis). Among critically ill patients, the use of acetate in hyperalimentation solutions is
an often unsuspected source.
Prolonged emesis and gastric suction are the two most
common causes in surgical patients. Both result in the loss
of chloride and protons from the stomach, producing alkalosis and volume contraction. The loss of blood volume
causes the secretion of renin and the production of aldosterone, which fosters sodium retention (to compensate for
volume loss) and potassium excretion. The decreased

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glomerular filtration rate (GFR) (in response to the decreased circulating blood volume) and the lowered potassium reset the kidney and allow complete reabsorption
of all filtered bicarbonate. A paradoxic aciduria may even
occur as the kidneys exchange protons for potassium.
The symptoms and physical findings associated with
mild metabolic alkalosis are usually nonspecific and are related to the underlying disorder that caused the alkalosis.
Alkalemia acts as a negative inotrope and can cause a decrease in blood pressure beyond that produced by the associated volume depletion. The increased pH also decreases the fraction of ionized serum calcium and reduces
the arrhythmia threshold. The leftward shift of the oxyhemoglobin dissociation curve reduces the amount of oxygen
unloaded and may contribute to tissue hypoxia.
Metabolic alkalosis should be treated with hydration.
Once normal renal function returns, potassium replacement is begun. This therapy increases the GFR and
causes the excretion of bicarbonate. In severe cases, or
when the alkalosis is not responsive to saline, acetazolamide (carbonic anhydrase inhibitor), arginine hydrochloride, or even 0.1 N HCl may be used. Acetazolamide results in renal loss of bicarbonate, potassium, water, and
sodium. The drug typically takes 23 days to produce an
effect and is normally begun intravenously at a dose of 5
mg/kg once daily.
Respiratory acidosis is present when there is an increased concentration of dissolved carbon dioxide [PaCO2]
in the blood. It most commonly occurs in patients with
chronic respiratory disease or in those receiving mechanical ventilation with insufficient minute ventilation. Other
causes include airway obstruction, respiratory center depression, circulatory collapse, neurogenic disease, and restrictive pulmonary processes. The increased PaCO2 is particularly problematic because dissolved carbon dioxide can
quickly cross membranes, such as the blood-brain barrier,
to alter metabolic processes. An acute change in PaCO2
produces a change in blood pH within about 10 minutes.
Buffering is by the nonbicarbonate system, which has a
large capacity; hence, only small changes in pH occur.
Once equilibrium is achieved, pH falls by about 0.08 units
for every 10-mmHg increase in PaCO2.
The symptoms of respiratory acidosis are nonspecific
and are usually related to the underlying cause. In severe
cases, fatigue, weakness, and confusion may be present.
Physical findings include tremor, asterixis, weakness, incoordination, papilledema, and pyramidal tract findings.
Coma may ensue when PaCO2 reaches 70100 mmHg.
Renal compensation causes a metabolic alkalosis by retaining bicarbonate, returning the pH toward normal.
As with all acid-base disturbances, the key to management revolves around identification of the underlying
process. For patients with acute or chronic respiratory
failure, this may include endotracheal intubation and mechanical ventilation. For those already receiving mechani-

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cal ventilation, the increased PaCO2 identifies inadequate

alveolar ventilation. This is caused either by improper
ventilator settings or by increased physiologic dead space.
Minute ventilation is the product of tidal volume and respiratory rate. The typical mechanically ventilated patient
requires 1015 ml/kg of tidal volume at 810 breaths/min.
Dead space is that proportion of inhaled volume that does
not come into contact with exchange surfaces of the lung.
Dead space has three components: apparatus, anatomic,
and physiologic. Anatomic dead space is that portion of
the ventilator volume that remains within the breathing
circuit, while anatomic dead space is that fraction that remains within the conducting airways, such as the trachea.
Physiologic dead space constitutes the largest and most
significant component and is caused by alveoli that have
lost either their normal perfusion or their ability to exchange gases. Normal dead space is 30% of tidal volume.
This may increase to more than 75% in extremely ill patients. Increased dead space produces a respiratory acidosis by reducing effective ventilation.
Respiratory alkalosis produces an alkalemia with decreased PaCO2 and a normal or decreased bicarbonate
concentration. Excitability and excessive mechanical ventilation are the most common causes. In the initial period
following injury, the response to pain causes a transient
respiratory alkalosis. The normal homeostatic response is
excretion of bicarbonate to produce a compensatory metabolic acidosis. In the steady state, the plasma bicarbonate
concentration falls by about 0.5 mEq/L for each 1-mmHg
decrease in PaCO2. The arterial pH is corrected toward,
but does not become, normal.
Symptoms of hyperventilation and severe respiratory
alkalosis include hypocalcemic tetany (due to the reduced
fraction of ionized calcium), irritability, anxiety, vertigo,
and syncope. ECG changes include ST segment or T wave
flattening and alterations in the QRS complex.
The key differential diagnosis of primary respiratory
alkalosis is from respiratory compensation for underlying
metabolic acidosis. Patients with severe underlying infections or diabetic coma often have respiratory compensation for their underlying acidosis.
Because respiratory alkalosis is always caused by hyperventilation, the key to treatment is the demonstration of the
underlying disorder. Blood gases will demonstrate whether
an associated hypoxia is the cause of hyperventilation. Drug
ingestions may also cause central nervous system excitement with hyperventilation. When the patient is receiving
mechanical ventilation, a reduction in the minute ventilation or change in the mode setting is usually curative.

K E Y

A drop in pH because of an increase in fixed acids is metabolic acidosis; when caused by accumulation of carbon dioxide,
it is respiratory acidosis; decreased hydrogen concentration (increased pH) is metabolic or respiratory alkalosis
Increase of 10 mmHg of carbon dioxide causes decrease in
pH of 0.8
Metabolic Acidosis
In metabolic acidosis, lactate accumulation produces lactic
acidosis
Symptoms of metabolic acidosis include Kussmaul respiration, decreased cardiac output, disorientation, lethargy, and
dehydration
Anion gap is composed of anions not normally measured in
routine laboratory determinations
Normal anion gap is less than 14 mEq/L; any decrease in bicarbonate concentration and/or increase in number of weak
acid salts widens gap and produces anion gap acidosis
Guiding principle in treatment of any metabolic acidosis is to
identify and correct underlying process
Base deficit is portion of acidosis or alkalosis due to a metabolic component
Amount of base required to achieve full correction of metabolic component of acidosis is calculated as mEq base required
+ 0.4 base deficit body weight (kg)
Rapid infusions of bicarbonate can produce profound respiratory acidosis in presence of respiratory failure in a spontaneously breathing patient
Metabolic Alkalosis
Decline in chloride does not compensate for rise in bicarbonate, so anion gap always decreases
Metabolic alkalosis produced by vomiting, prolonged gastric
suction, use of diuretics, and volume depletion (contraction
alkalosis)
Prolonged emesis and gastric suction the two most common
causes in surgical patients
Alkalemia acts as a negative inotrope and can cause a decrease in blood pressure beyond that produced by associated
volume depletion
Respiratory Acidosis
Increased PaCO2 particularly problematic because dissolved
carbon dioxide can quickly cross membranes, such as bloodbrain barrier, to alter metabolic processes
Once equilibrium achieved, pH falls by about 0.08 units for
every 10-mmHg increase in PaCO2
For patients with acute or chronic respiratory failure, management includes endotracheal intubation and mechanical
ventilation

P O I N T S

Decreased bicarbonate or increased protons results in acidosis; increased bicarbonate or decreased protons results in
alkalosis

Respiratory Alkalosis
Respiratory alkalosis produces alkalemia with decreased
PaCO2 and normal or decreased bicarbonate concentration;

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excitability and excessive mechanical ventilation are most common causes

Symptoms of hyperventilation and severe respiratory
alkalosis include hypocalcemic tetany (due to reduced fraction of ionized calcium), irritability, anxiety, vertigo, and
syncope
Key differential diagnosis of primary respiratory alkalosis is
from respiratory compensation for underlying metabolic
acidosis

SUGGESTED READINGS
Bongard FS, Sue DY: Fluid, electrolytes, and acid base. In
Bongard FS, Sue DY (eds): Current Critical Care Diagnosis and Treatment. Appleton & Lange, E. Norwalk, CT,
1994.
A good chapter with ample detail on fluid and electrolyte
disturbances. Contains many of the charts and nomograms
that appear in Cogan (see below).
Cogan MG: Fluid and Electrolytes: Physiology and Pathophysiology. Appleton & Lange, E. Norwalk, CT, 1991
A monograph that includes detailed physiologic descriptions
of acid-base disorders. It should be used as a reference when
detailed information about complex acid-base disorders is
needed. It contains several nomograms and charts that may
be helpful in diagnosing these disorders.

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QUESTIONS
1. Hypernatremia?
A. Always occurs in the presence of volume
contraction.
B. Should be treated whenever present.
C. Usually occurs in the face of metabolic alakalosis.
D. Causes an increase in the serum osmolality.
2. Potassium?
A. Is largely an extracellular cation.
B. Is increased in patients with metabolic alkalosis.
C. Can be replaced rapidly in deficiency states.
D. Produces U waves on the ECG in decreased
concentration.
3. Metabolic alkalosis?
A. Increases the delivery of oxygen to the tissues.
B. Increases the fraction of ionized calcium.
C. Commonly occurs following prolonged gastric
suction.
D. Is not related to the concentration of potassium.
4. Increased physiologic dead space?
A. Produces a metabolic alkalosis.
B. Produces a respiratory alkalosis.
C. May require an increased minute ventilation to
treat.
D. Is associated with diuretic use.
(See p. 603 for answers.)

MANAGEMENT
OF CASE 2
A P P E NDI X 2 . 1

ase 2 illustrates the inadvertent creation of hyponatremia, the most common postoperative fluid and electrolyte disturbance. This was caused by the use of a solution containing only D5W + 20 mEq KCl/L, instead of a
more physiologic solution (e.g., D5W + 12NS + 20 KCl)
for maintenance.
The patients operation took 5 hours, during which
time she lost 1 L of blood. Evaporation (insensible) from
the peritoneal and visceral surfaces is a major cause of
fluid loss during laparotomy. Normally, this loss is replaced
by the anesthesiologist with either saline or lactated
Ringers solution at 10 ml/kg/hr. Although this may seem
like a large volume, evaporative loss can be considerable.
Blood loss during surgery is replaced either with blood
(depending on how much is lost and on any pre-existing
conditions such as ischemic cardiac disease) or with balanced salt solution (normal saline or lactated Ringers) in a
ratio of 3 ml crystalloid (crystalloid is a term applied to any
solution that does not contain high-molecular-weight molecules such as albumin) for each milliliter of blood lost.
Colloids, which do contain high molecular weight species,
can be used in smaller volumes. Colloid solutions are expensive and offer no real advantages. The 3:1 ratio is required, as most of the replacement solution quickly leaves
the intravascular space to enter the interstitium. Using
these guidelines, the patient should have received:
Maintenance (open abdomen):
10 ml/kg/hr 5 hr 50 kg
1,000 ml blood loss 3 ml replacement/ml
blood lost
Expected intraoperative replacement
16

2,500 ml
3,000 ml
5,500 ml

From this calculation, we can see that the 5 L of lactated Ringers solution received in the operating room was
appropriate.
To write the postoperative fluid orders, we need to
consider three factors: (1) pre-existing loss, (2) maintenance requirements, and (3) ongoing loss.
1. Pre-existing loss
Our calculation indicates that she may have received
about 500 ml too little during surgery. If we follow the
rule about the time required for replacement, one-half
(250 ml) should be given over the first 8 hours (about
30 ml/hr), with the remainder given over the next 16
hours (250 ml/16 hr = 15 ml/hr). These are relatively
small volumes and, since we are primarily concerned
about the free water lost from evaporation, we can use
the maintenance fluid chosen to replace this loss rather
than use a separate solution.
2. Maintenance Requirement
This can be calculated simply using our estimate for
fluid requirement in a 50-kg patient.
100 ml/kg for the first 10 kg
1,000 ml
50 ml/kg for the next 10 kg
500 ml
20 ml/kg for each remaining kg
600 ml
Total 24-hr requirement
2,100 ml (or 90 ml/hr)

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3. Ongoing loss
Although this patient does not have any drains in place,
we know that a paralytic ileus will form (following manipulation of the bowel) and that fluid will leak into the
bowel lumen. This third spacing can constitute considerable loss and must be accounted for. Table 2.1 indicates that the volume (primarily small bowel) can be as
much as 2,0003,000 ml/24 hr with a composition similar to that of lactated Ringers or 12NS + 20 mEq KCl, to
which bicarbonate has been added to account for the
extra sodium and bicarbonate present. We will estimate
the loss at 1,200 ml/day (since we are not draining the
entire small bowel, it seems reasonable to begin with a
smaller volume), which would require 50 ml/hr.
Adding the requirements:
Pre-existing loss (using lactated
Ringers solution)
Maintenance
Ongoing loss (using lactated
Ringers solution)
Total fluid requirement

30 ml/hr (8 hr)
90 ml/hr
50 ml/hr
170 ml/hr (8 hr)

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Because lactated Ringers solution will serve to replace

both the pre-existing and the ongoing losses, we should
consider its use for the maintenance fluid as well. It is
somewhat higher in sodium that D5 12 NS, but its use for
24 hours (during which time the pre-existing loss is replaced) will result in only a relatively small excess of
sodium, after which time we can change to a more dilute
sodium solution. Therefore, our initial fluid order would be
D5 lactated Ringers solution at 170 ml/hr for 8 hours, followed by D5 lacted Ringers solution at 155 ml/hr for the
next 16 hours. At 24 hours, we can change to D5W 12 NS +
20 mEq/KCl at 140 ml/hr and adjust the rate depending on
the patients urine output. Daily review of the serum electrolytes (especially sodium and bicarbonate) will guide
changes in this regimen. The complications sustained by
the patient were due to hyponatremia: paralytic ileus, muscle irritability, and seizures. These would have been prevented had the calculations obtained been used instead.