Journal of Parenteral and Enteral

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Fluid and Electrolyte Management: Putting a Plan in Motion

Kristen M. Rhoda, Mary Jo Porter and Cristiano Quintini
JPEN J Parenter Enteral Nutr 2011 35: 675
DOI: 10.1177/0148607111421913

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Tutorial
Fluid and Electrolyte Management:
Putting a Plan in Motion
Kristen M. Rhoda, MS, RD, CNSD1;
Mary Jo Porter, RD, CNSC1; and Cristiano Quintini, MD1
Financial disclosure: none declared.
Fluid and electrolyte management is challenging for clinicians,
as electrolytes shift in a variety of settings and disease states and
are dependent on osmotic changes and fluid balance. The devel-
opment of a plan for managing fluid and electrolyte abnormali-
ties should start with correcting the underlying condition. In
most cases, this is followed by an assessment of fluid balance
with the goal of achieving euvolemia. After fluid status is under-
stood and/or corrected, electrolyte imbalances are simplified.
Many equations are available to aid clinicians in providing safe
recommendations or at least to give a starting point for correct-
ing the abnormalities. However, these equations do not take into
consideration the vast differences between clinical scenarios,
thus making electrolyte management more challenging. The
Preface
Learning fluid and electrolyte management as a dietitian
was a complex undertaking. Attempting to remember all of
the information from biochemistry textbooks and intern-
ship preceptors seemed impossible when I encountered
my initial “real life” scenario. Following the steps laid out
for me as a student helped, but it was the expertise shared
from physicians, pharmacists, nurses, and dietitians within
the multidisciplinary team that advanced my knowledge.
Tackling a potassium (K) imbalance is never as simple as
administering a K bolus. Treatment requires understand-
ing the pathophysiology of the disease or condition that
leads to the imbalance with the assistance of the physi-
cian, applying the principles of pharmacokinetics with the
support of the pharmacist, understanding medication
delivery tactics and vascular access selection criteria with
the aid of the nurse, and applying nutrient absorption and
From the 1Intestinal Rehabilitation and Transplant Program,
Center for Human Nutrition, Cleveland Clinic, Cleveland, Ohio.
Received for publication July 23, 2011; accepted for publication
August 9, 2011.
Address correspondence to: Kristen M. Rhoda, MS, RD, CNSD,
Intestinal Rehabilitation and Transplant Program, Center for
Human Nutrition, Cleveland Clinic, 9500 Euclid Ave/A100,
Cleveland, OH 44195; e-mail: kristen.rhoda@gmail.com.
675
Journal of Parenteral and
Enteral Nutrition
Volume 35 Number 6
November 2011 675-685
© 2011 American Society for
Parenteral and Enteral Nutrition
10.1177/0148607111421913
http://jpen.sagepub.com
hosted at
http://online.sagepub.com
supplementation plan, whether delivered intravenously or orally,
must include an assessment of renal and gastrointestinal func-
tion, as most guidelines are established under the assumption of
normal digestion, absorption and excretion. After the plan is
developed, frequent monitoring is vital to regain homeostasis. A
fluid and electrolyte management plan developed by a multidis-
ciplinary team is advantageous in promoting continuity of care
and producing safe outcomes. (JPEN J Parenter Enteral Nutr.
2011;35:675–685)
Keywords:  electrolytes; fluid; multidisciplinary team; osmolality;
hyponatremia
metabolism with the help of the dietitian. Our Intestinal
Rehabilitation and Transplant Program represents a refer-
ral center for patients with advanced and complex intesti-
nal failure. Chronic diarrhea, dehydration, electrolyte
abnormalities, micronutrient imbalances, and malnutri-
tion exist often in the context of renal dysfunction, ongo-
ing inflammatory state, and the result of a major
gastrointestinal (GI) anatomical derangement (just as in
“combinatorial mathematics,” in which a derangement is
a permutation of the elements of a set such that none of
the elements appear in their original position). Whether
the patient is on specialized nutrition support or taking in
a modified diet, using the skills provided by the multidis-
ciplinary team assists in my ability to dissect operative
reports, interpret GI and vascular imaging studies, assess
medication history, and determine the underlying etiology
of malabsorption. This approach is, in my opinion, the
single most important determinant for success.
Introduction
Fluid and electrolyte management is challenging to most
clinicians, as each clinical picture is ever changing. The
following article summarizes the primary function and
regulatory mechanism of each electrolyte. Assessment
tactics and treatment guidelines are also reviewed. The
purpose of this article is to provide a thorough review of
676   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 6, November 2011
Table 1.   Useful Equations in Calculation of Fluid and Electrolyte Needs1,4-8
Sodium deficit or excess (mEq)
Normal TBW
a
Current TBW
Amount of water needed to return serum Na to 140 mEq
Serum osmolality (mOsm/kg)
Change in serum Na concentration with 1 L of IVF solution
*= mEq of Na/L of solution
Example:
1L 0.9% NS = 154 mEq/L
Prediction of serum sodium for hyperglycemia
Corrected Mg
Corrected Ca
Prediction of fluid requirements for fever
Ca, calcium; K, potassium; Mg, magnesium; NS, normal saline; Na, sodium; TBW, total body water.
a
Formula underestimates the TBW deficit in cases with hypotonic fluid loss requiring additional Na and K repletion.
fluids and electrolytes. As with most topics within clinical
practice, additional reading is encouraged to improve
baseline knowledge of electrolyte management.
Water
Water is a major component of the human body. Total
body water (TBW) constitutes approximately 45%–60% of
body weight and is divided into extracellular fluid (ECF)
and intracellular fluid (ICF) compartments.1 ICF accounts
for two-thirds of TBW, which accounts for up to approxi-
mately 40% of body weight, with the remaining one-third
of TBW being ECF, accounting for approximately 20% of
body weight.1 ECF encompasses intravascular fluid,
interstitial fluid, and transcellular fluid (contained within
certain body cavities).2 Examples of transcellular fluid
include GI, cerebrospinal, pleural, and intraocular fluids.
Although transcellular fluid makes up only a small por-
tion of fluid in adults (˜1 L), it accounts for a great
amount of water movement in and out of the transcellular
fluid.1-3 Water moves between the ICF and ECF compart-
ments depending on the amount of solutes present until
it reaches a state of equilibrium. The measurement of this
movement is referred to as osmolality and is often used
interchangeably with tonicity. Osmolality is measured in
milliosmoles per kilogram (mOsm/kg) of water. The osmo-
lality of body fluids and isotonic fluids is approximately
280–300 mOsm/kg. Assessment of serum and urine
osmolality can guide the treatment of TBW imbalances
(see Table 1). Water excretion is primarily regulated
through glomerular filtration, tubular reabsorption and
= (140-serum Na) × TBW
= 0.6 × kg body weight
= (normal serum Na × TBW)/Measured serum Na
= sodium excess/140
= (2 × serum Na) + (serum urea mg/dL/2.8) +
(blood glucose mg/dL/1.8)
= (*mEq/L – serum Na)/TBW + 1
Example: = (154 mEq/L – 123)/41.9
= 0.74 mEq change in serum sodium with 1 L NS infusion
= blood glucose (mg/dL) × 0.016 + serum Na
= Mg in mEq/L + 0.005 (40 – albumin g/L)
= ([4 – serum albumin (g/dL)] × 0.8) + measured calcium (mg/dL)
= 12.5% increase in fluid needs for each degree >37°C
secretion, and water conservation within the nephron
loop.9 TBW loss occurs through urine (500–1,500 mL/d),
GI losses (100–200 mL/d), skin
(300 mL/d), and the respiratory tract (400 mL/d).2,10
Understanding normal TBW loss is important when cal-
culating the estimated fluid requirements.
Following is an example of estimated fluid require-
ments for an adult with normal renal function.2 A 46-year-
old man with an average ileostomy output of 1,800 mL,
1,000 mL oral fluid intake, and 2,000 mL intravenous
fluid (IVF) per day, over the past week, with a Tmax of
38.5°C. Daily fluid requirements are:
+ 1,500 mL for urine
+ 1,800 mL for stoma output
+ 500 mL insensible
+ 500 mL fever (see Table 1)
– 1,000 mL oral intake
– 2,000 mL IVF provision
= 1,300 mL estimated fluid requirements
Hypovolemia. Hypovolemia, defined as an ECF deficit,
may occur as a decrease in water volume, with or without
an electrolyte deficit.1,3 Hypovolemia as a water deficit
alone is usually the result of an inability to regulate water
intake (eg, lost of the thirst mechanism or concentrated
enteral nutrition). Pathognomonic signs of hypovolemia
include thirst, dizziness, hypotension, tachycardia, poor
skin turgor, and decreased urinary sodium (Na) concen-
tration (<15 mEq/L).1 Chemical abnormalities reveal
hypernatremia; however serum Na levels do not reflect
total Na levels but rather serve as an indicator of the

Table 2.   Commonly Used Intravenous Fluids
Source Na Cl
NS 154 154
D5W 0 0
D5, 0.45NS 77 77
D5, 0.9NS 154 154
LR 130 109
D5, LR 130 109
Cl, chloride; D5, 5% dextrose solution; D5W, 5% dextrose solution in water; K, potassium; LR, Lactated Ringers; Na, sodium; NaCl,
sodium chloride; NS, normal saline.
osmolality of the serum.1,3,10 In this scenario, treatment is
aimed at replacing water, with the goal of regaining Na
homeostasis and serum osmolality. IVF replacement
should be administered as 5% dextrose in water,11 or in
the case of (orthostatic) hypotension, a hypotonic solu-
tion should be given (see Table 2). Hypovolemia, with a
combined water and electrolyte deficit, is the result of
excessive losses (eg, GI losses, diuretic therapy, or postop-
erative fluid sequestration). Chemical abnormalities are
not as reliable in this scenario and will vary depending on
the type of fluid loss. Volume depletion results in
decreased urinary Na concentration (<10 mEq/L),
increased plasma osmolality (driven by hypernatremia),
and increased urine osmolality (>450–500 mOsm/kg).1
Elevated plasma osmolality stimulates the secretion of
antidiuretic hormone (ADH) to increase water reabsorp-
tion in the renal tubules. The calculation of Na and vol-
ume deficit determines the need for fluid and electrolyte
replacement. An isotonic solution such as normal saline
(NS) is often indicated in these cases.1,11
ADH is one of 6 hormones that affect water and elec-
trolyte balance. Others include angiotensin II, aldoster-
one, cortisone, epinephrine, and norepinephrine. ADH is
an arginine vasopressin produced in the pituitary gland,
which controls renal excretion and reabsorption of water.
Osmoreceptors located in the hypothalamus are sensitive
to changes in serum osmolality and trigger the release or
suppression of ADH upon detection of hyperosmolality
and hypoosmolality, respectively. Upon detection of
hyperosmolality, ADH is released, alerting the kidney to
reabsorb water, which subsequently decreases serum
osmolality.12 Excessive water reabsorption leads to hypoos-
molality, and the osmoreceptors respond by shutting off
ADH secretion. Secretion of ADH during hypoosmolality
and normal blood volume is referred to as the syndrome
of inappropriate ADH hypersecretion (SIADH). SIADH
results in increased reabsorption of water, leading to
worsened hypoosmolality, hyponatremia, and hypoten-
sion.12 SIADH develops in response to central nervous
system diseases, stress response during the postoperative
period, and pulmonary diseases.3,12 It is diagnosed based
on the clinical findings of hyponatremia, serum hypoos-
Fluid and Electrolyte Management / Rhoda et al   677
K+ Lactate Dextrose mOsm
0 0 0 280–300
0 0 50 250
0 0 50 400
0 0 50 560
4 28 0 270
4 28 50 525
molality, euvolemia, and urinary hyperosmolality (>100
mOsm/kg of water), in the presence of normal thyroid
and adrenal function.12 Treatment should be aimed at
correcting the primary problem, along with water restric-
tion and Na replacement. Vasopressin-receptor antago-
nists are also used to help inhibit the action of ADH.3,12
Hypervolemia. Hypervolemia is defined as ECF volume
expansion, and may occur due to altered renal function,
excessive fluid administration, interstitial to plasma fluid
shift, or post-operative stress response.1,3 Hypovolemia
is often seen after surgery and anesthesia, as ADH is
released, resulting in water retention by the kidneys. This
condition may be worsened by heart failure, hypoalbu-
minemia, and liver or renal disease.1 Pathognomonic
signs of hypervolemia include edema, increased body
weight, jugular venous distention, tachypnea, and hyper-
tension.1-3 Chemical abnormalities reveal hyponatremia
and hypo-osmolality, requiring Na restriction to prevent
worsening water retention. If the patient is hypervolemic
and hyponatremic, both free water and Na should be
restricted.1 In some cases, the use of diuretics can aid in
mobilization of fluid.13
Na
Na is found predominantly in ECF and strongly contrib-
utes to osmolality and the regulation of acid-base bal-
ance.1,3,5 Plasma Na concentration does not reflect total
body Na but is an indicator of extracellular volume sta-
tus.2 Na balance is regulated by the kidney through the
excretion and reabsorption of Na and water in the distal
tubule and loop of Henle.6
Hyponatremia. Hyponatremia (plasma [Na+] <135
mEq/L) may be classified as either hypotonic (dilutional)
or non-hypotonic.14 Nonhypotonic hyponatremia may
result from a shift of fluid out of cells and into ECF,
resulting in serum hyperosmolarity and dehydration of
the cells. The most common form of hyponatremia is
hypotonic (dilutional) hyponatremia due to an excess of
678   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 6, November 2011

Table 3.   Presentation of Electrolyte Depletion With Corresponding Pathophysiology7,10,14,15

Signs and Symptoms Pathophysiology

Calcium 1. Hyperactive reflexes, light-headedness, irritability, 1. D

 ue to increased excitability of nerve and muscle
seizures, hyperventilation cells
2. Tetany, numbness with tingling of fingers 2. D
 ue to spontaneous skeletal muscle contractions that
occur repeatedly
Phosphorus 1. Confusion, seizures, coma 1. Reduced oxygenation of the myocardium
2. Chest pain 2. Cardiac muscle has less ATP, which decreases
3. Difficulty breathing cardiac output and BP and increases pulmonary
4. Weakness wedge pressure
5. Bone pain 3. Decreased 2,3-diphosphoglycerate and ATP in RBC
6. Bruising, bleeding 4. Lack of P and ATP in muscle causing less strength
7. Respiratory dysfunction with muscle contraction
5. Changes in P and ATP deficits increase bone resorption
and osteomalacia and lower bone Ca, P, Mg
6. Due to platelet dysfunction
7. D ecreased availability of phosphate-containing
energy sources

Magnesium 1. Weakness, lethargy, muscle cramps 1. I ncreased update of calcium causing tension of
2. Mood changes, confusion vascular smooth muscle
3. Vomiting, decreased cardiac output 2. CNS changes
3. Increased update of calcium causing tension of
vascular smooth muscle

Sodium 1. Nausea, vomiting, headache, muscle cramps, 1. Related to serum osmolality changes in the CNS
disorientation, weakness, lethargy, confusion,
dizziness, seizure, coma, death

Potassium 1. Constipation 1. Caused by smooth muscle weakness

2. Weakness 2. Due to an increased ratio of intra- to extracellular K
3. Lethargy
4. ECG abnormalities
ATP, adenosine triphosphate; BP, blood pressure; Ca, calcium; CNS, central nervous system; ECG, electrocardiogram; K, potassium;
Mg, magnesium; P, phosphorus; RBC, red blood cell.

water.14 Hyperglycemia may worsen hyponatremia, by
increasing serum osmolality, which in turn generates a
shift of water into the ECF, thus decreasing serum Na
concentration. Hyperglycemia decreases serum Na by 1.7
mEq/L when hyperglycemia exceeds 100 mg/dL14 (see
Table 1). Hypokalemia may also worsen hyponatremia
because of the extracellular and intracellular ratio
required to maintain homeostasis.14
Treatment of hyponatremia starts with water restric-
tion and should be guided by the severity of symptoms
(see Tables 3 and 4) and evaluation of the length of time
in which hyponatremia developed (see Table 1). Acute
onset of hyponatremia, occurring in <48 hours, requires
correction of serum Na with isotonic IVF (e.g., NS) at a
rate of 1–2 mEq/L/h. Patients with severe symptoms such
as seizures or mental changes, along with concentrated
urine >200 mOsm/kg and plasma Na <120 mEq/L, who
are euvolemic or hypervolemic require serum Na cor-
rected at a rate of 1–2 mEq/L/h using hypotonic saline
(eg, ½ NS).14 Chronic hyponatremia, occurring over 2–3
days or longer, should be given isotonic IVF to correct
serum Na at a rate of ≤0.5 mEq/L/h while monitoring
serum Na to not exceed 8–12 mEq/L in 24 hours (see
Table 1). As a general rule, approximately 50% of the esti-
mated Na deficit should be given in the first 24 hours,
with the remainder given over the next 24–72 hours.
Goals for treatment should not exceed a rise in serum Na
>135 mEq/L with initial correction, and for severe
hyponatremia (<105 mEq/L), the goal is to reach a serum
Na level of 120–130 mEq/L (see Table 1). Lab monitor-
ing of serum Na should occur every 2–4 hours when the
patient is symptomatic and every 4–8 hours when asymp-
tomatic.2,7 Slow treatment of hyponatremia is crucial in
preventing osmotic myelinolysis (see Tables 3 and 4).16
Hypernatremia. Hypernatremia (>145 mEq/L) is usually
due to a water deficit leading to cellular dehydration but
may also result from excessive Na, which is usually a
result of iatrogenic Na administration.4 Treatment begins
with an evaluation of body water deficit (see Table 1).
Acute hypernatremia requires rapid correction with a
decrease in plasma Na concentration of 1 mEq/L/h.5 In
chronic hypernatremia, treatment should be aimed at
lowering plasma Na at a rate of 0.5 mEq/L/h, with a

Table 4.   Presentation of Elevated Electrolytes With Corresponding Pathophysiology5,10
Signs and Symptoms
Calcium 1. Anorexia, nausea, vomiting
2. Polyuria, stones, nocturna, uremia
3. Confusion, coma, incontinent
4. Weakness, fatigue
Phosphorus 1. Anorexia, nausea, vomiting, oliguria, corneal
haziness, conjunctivitis
2. Tetany
3. Hypocapnia
4. Hyperactive reflexes
5. Tachycardia
6. Muscle weakness
Magnesium 1. Nausea, vomiting, diaphoresis, muscle weakness
2. Altered mental status, coma, lethargy, confusion
Sodium 1. Increased thirst, fatigue, restlessness, muscle
irritability, seizures, coma, death
Potassium 1. Muscle weakness, flaccid paralysis
2. ECG changes
3. Muscle cramping
4. Arrhythmias
CNS, central nervous system; ECG, electrocardiogram; K, potassium.
maximum decrease of 10 mEq/L/d. Serum Na reduction
should not exceed 1 mEq/L/h, or cerebral edema and
death may result (see Table 1).2,3
K severely malnourished patient leads to life-threatening
K is the primary intracellular cation, with only 2% of total
body K (TBK) remaining in the ECF. Cellular metabo-
lism, specifically protein and glycogen synthesis, depends
on sufficient intracellular K concentration. Optimal TBK
promotes neuromuscular and cardiac function as well.
Maintaining an intracellular to extracellular ratio of
approximately 30:1 is essential to life, as a 1.5%–2%
variation can lead to fatal consequences.6 Because of this
precise balance of K in the ICF and ECF, both renal and
nonrenal mechanisms contribute to the maintenance of
TBK.
The kidneys play a major role in maintaining K home-
ostasis. Renal K secretion takes place in the distal neph-
ron and is driven by aldosterone balance.1 Although many
factors drive aldosterone secretion, the effect of serum K
levels on aldosterone secretion is significant. As K con-
centration climbs, aldosterone secretion increases, caus-
ing the distal tubule and collecting duct to reabsorb Na
and secrete K.1 The opposite occurs in the presence of
hypokalemia. Medications, especially diuretics and neph-
rotoxic drugs, can affect urinary K excretion and therefore
should be adjusted accordingly during a K imbalance.1,6,17
While the kidney is the main regulatory organ for
maintaining K homeostasis, nonrenal mechanisms such
as hormones, pH, osmolality, and adaptation also play an
Fluid and Electrolyte Management / Rhoda et al   679
Pathophysiology
1. Decreased activity of the gastrointestinal muscles
2. Decreased activity of urinary muscles
3. Decreased CNS activity
4. Due to decreased activity of nerve and muscle cells
1. Metastatic calcifications
2. Hypocalcemia
3. Hypoxemia
1. Neuromuscular
2. Central nervous system
1. Related to serum osmolality changes in the CNS
1. Decreased ratio of intra- to extracellular K
2. R
 epolarization of the ventricles and depolarization of
the atria and ventricles
important role. It is well known that insulin secretion
promotes the movement of K from the ECF to the ICF,
but the mechanism is the subject of continued debate.1
This is particularly relevant in refeeding syndrome, as an
insulin surge after the reintroduction of nutrition in a
hypokalemia.18-20 In acidosis, hydrogen ions move into the
ICF to be buffered, which forces K, an equivalent cation,
into the ECF.1 Therefore, as pH changes, there is a recip-
rocal change in K. Osmolality is another driving force for
maintaining K balance, as an elevated plasma osmolality
causes fluid to shift into the ECF.1 This shift increases
the intracellular K content, which leads to hyperkalemia.
Lastly, K adaptation refers to the ability to decrease cel-
lular uptake, when excessive exogenous K is given, and/or
when TBK is elevated.1 This adaptation is a preventative
measure against the development of life-threatening
hyperkalemia.
The dietary reference intake (DRI) for adults >18
years of age is established at 4.7 g/d and at 1–2 mEq/kg/d
for parenteral nutrition (PN)–dependent individuals and
then adjusted as needed.6 The small intestine absorbs
approximately 90% of dietary K, and a trivial amount of K
absorption occurs in the colon.21 After dietary K is absorbed,
the kidneys regulate urinary excretion and reabsorption.
Hypokalemia. Assessing hypokalemia (serum K <3.5
mmol/L) is also a complex task since many factors con-
tribute to its imbalance. In addition to assessing renal
function, medications, and exogenous intake, magnesium
(Mg) status should also be assessed. Mg plays a vital role
in the maintenance of the Na-K adenosine triphosphate
680   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 6, November 2011
(Na-K-ATPase) pump, which regulates the intracellular to
extracellular K ratio.22 In cases of hypokalemia with con-
current hypomagnesemia, Mg levels must be repleted
prior to correcting the K imbalance.6,15,22
As with hyperkalemia, dietary intake is rarely the
cause of the hypokalemia, and therefore, increasing die-
tary intake is unlikely to improve serum K levels. Treatment
should be based on 2 factors: the presence of symptoms
(see Tables 3 and 4) and serum K levels (see Table 5).
Oral K supplementation is appropriate for asymptomatic,
mild hypokalemia (K 3.2–3.5 mmol/L). Symptomatic and/
or severe hypokalemia (K <3.0 mmol/L) requires intrave-
nous (IV) supplementation. In either case, medications,
which may be contributing to excessive urinary K losses
(eg, furosemide), should be adjusted. Potassium chloride
(KCl) is preferred for correction of alkalosis or improve-
ment of extracellular volume expansion. In cases of acido-
sis, potassium acetate may be a better choice.
Hyperkalemia. Assessing hyperkalemia (serum K >5
mmol/L) is challenging, but its difficulty can be lessened
if handled in a systematic way. First, pseudohyperkalemia
should be ruled out prior to any treatment. Pseudohyper-
kalemia is defined by the presence of hemolysis, extreme
leukocytosis, or thrombocytosis resulting in false hyperka-
lemia.26 After pseudohyperkalemia is ruled out, renal
function, medications, and exogenous intake need to be
assessed prior to treatment.
Treatment for hyperkalemia starts with the reduction
of dietary K and promotion of optimal urinary output
(>1,000 mL/d). Medications that could be contributing to
decreased urinary K excretion (eg, spironolactone, non-
steroidal anti-inflammatory drugs, heparin, β-blockers,
and digitalis; see Table 5) require adjustment. Persistent
hyperkalemia requires the use of a resin (eg, Na polysty-
rene sulfunate) to produce a cathartic effect.17 Caution
must be taken when using a resin to prevent rebound
hypokalemia, as the K may take several hours to normal-
ize. For life-threatening levels (K >8.0 mmol/L), institu-
tional algorithms for the use of calcium (Ca), bicarbonate,
dextrose with insulin, and hypertonic saline to correct
hyperkalemia should be followed (see Table 5).
Mg
Mg is the second most abundant intracellular cation.
Total body Mg is present in bone (60%–65%), skeletal
muscle (20%), and nonmuscular tissue (11%), leaving
only a small amount of interchangeable Mg (<1%) within
the ECF.15
Mg functions in >100 enzymatic reactions and is
involved in cellular energy metabolism.1,15 Serum Mg is a
poor indicator of total body stores yet remains the stand-
ard measurement because of the complexity of alternative
evaluation methods.27 Approximately 25% of Mg is pro-
tein bound, bringing to question the possible benefit of
using ionized Mg levels and/or using an equation for
hypoalbuminemia (see Table 1). Despite conflicting
reports, serum ionized Mg has not yet proven to be a
superior method of detecting Mg deficiency and/or pre-
dicting clinical outcomes.27 The Mg tolerance test involves
the measurement of 24-hour renal excretion, before and
after PN Mg administration. Retention of >20% of Mg
indicates a deficiency.27 Although this test is considered
accurate, it is not realistic in hospitalized patients because
of the complexity of collecting urinary samples.
Mg absorption is primarily regulated by GI and renal
mechanisms.10 The DRI for adults >18 years of age is
410–420 mg/d for men, 310–360 mg/d for women,28 and
approximately 8–20 mEq/d6 for PN-dependent individuals.
Approximately 30%–40% of dietary Mg is absorbed by the
GI tract, and the remainder is excreted in stool. GI absorp-
tion occurs primarily in the jejunum and ileum, with some
absorption also occurring in the colon.15,27 Intestinal
absorption may be reduced by excessive zinc, vitamin B6,
oxalates, and free fatty acids.15,27 Hypomagnesemia blocks
the release of Ca from within the cell and impairs the
secretion of parathyroid hormone (PTH), both of which
lead to hypocalcemia.10,29 Mg is necessary for intracellular
and extracellular movement of K via the Na-K-ATPase
pump; thus, Mg levels should be corrected to subsequently
enable repletion of K and Ca.15
Mg excretion is a function of the kidney, with most
reabsorption occurring in the ascending loop of Henle.15,27
The kidneys have the ability to conserve Mg during states
of deficiency. It is important to understand that the maxi-
mum tubular reabsorption in the loop of Henle decreases
with an increased Mg load. Tubular reabsorption is
dependent on serum Mg levels, the Mg dose, and Mg
infusion.10 Within the proximal tubule, hypercalcemia
results in an increased excretion of Mg,27 while phosphate
depletion prevents reabsorption within the ascending
limb and distal tubule.15
Hypomagnesemia. Hypomagnesemia (<1.5 mEq/L) devel-
ops in a variety of settings, including increased GI or urinary
losses, chronic alcohol abuse, and hyperaldosteronism.1,3,27
Hypomagnesemia is also seen during refeeding syndrome,
due to intracellular shifting of Mg, total body depletion,
and increased demand of Mg for anabolism.18 Treatment
is determined based on the presence of symptoms (see
Tables 3 and 4) and on the serum level. Oral supplementa-
tion is warranted with mild Mg (defined as 1.1–1.4 mg/
dL). Symptomatic or severe hypomagnesemia (<1 mg/dL)
should be replaced with 32–64 mEq of IV Mg. Oral
supplementation with Mg salts is available in a variety
of preparations. Caution must be taken as large doses of
oral Mg and, in particular, Mg oxide salts have been
shown to increase osmotic load, resulting in diarrhea.6
 Fluid and Electrolyte Management / Rhoda et al   681

Table 5.   Treatment Considerations for Electrolyte Abnormalities6,7,17,23-25

Electrolyte Elevation Depletion

Calcium Oral Oral

Low-calcium diet 1,000–1,500 mg/d
Reduce vitamin A, vitamin D, and/or calcium- IVb (tetany present)
containing antacids 10–20 mL of 10% calcium gluconate IV
IV over ≥4 hours
Start NS at 200–300 mL/h; may need to start
furosemide IV when rehydrated
Phosphorus Oral Oral (mild replacement)
Low-phosphorus diet Increased dietary intake or
Phosphate binders Consider phosphate-containing multivitamin
IV IV (moderate replacement)
Assess the need for volume repletion Oral supplementation: 2.5–3.5 g/d in divided doses
Dialysis may be needed in severe cases 0.32–0.64 mmol/kg IV (max 30 mmol Na3PO4) slowly
over 6 hours
IV (severe replacement)
1 mmol/kg IV (max 80 mmol Na3PO4) slowly over
8–12 hours
Magnesium Oral Oral (mild)
Remove magnesium-containing medications Increase dietary intake
Consider starting diuretics Oral supplementation (eg, magnesium lactate)
IV (severe >12.5–32 mg/dL) IV (moderate)
Start 10 mL of a 10% calcium gluconate solution in 8–32 mEq (max 1.0 mEq/kg) slowly with 8 mEq over
severe cases 1–2 hours daily
7.8-13.6 mEq Ca via central infusion over 5–10 IV (severe <1 mg/dL)
minutes or 4.56–12.7 mEq Ca peripherally 32–64 mEq (max 1.5 mEq/kg) slowly with 8 mEq over
over 3–10 minutes 1–2 hours daily
Sodium Oral Oral
Low-sodium diet Consider free water restriction
Increase oral fluid intake IV (mild to moderate)
IV Consider free water restriction
Decrease or discontinue administration of sodium Provision of ½ NS and/or NS (correct at a rate of
with replacement of water deficit 1–2 mEq/L/h)
IV (severe)
3% sodium chloride (correct at a rate of 1–2 mEq/L/h)
Potassium Oral Oral
Low-potassium diet Increase dietary intake and/or add salt substitutes
Remove potassium-sparing medications Oral supplementation: 40–100 mEq daily in divided
Consider use of diuretics doses
IV (nonsymptomatic) IVa (mild)
Sodium bicarbonate (50–100 mEq) 40 mEq PO × 1 or
Dextrose infusion (25–100 g with 5–10 units 10 mEq IV over 1 hours × 3–4 doses
insulin) IVa (moderate)
IV (symptomatic) 20 mEq PO every 2 hours × 3 doses or
Calcium gluconate (1–2 g) 10 mEq IV over 1 hour × 4 doses, recheck and repeat
as needed
IVa (severe)
40 mEq IV over 2–4 hours, recheck and repeat as
needed or
40 mEq IV over 4 hours as needed
Ca, calcium; IV, intravenous; Na3PO4, sodium phosphate; NS, normal saline; PO, per os.
a
Not to exceed 20 mEq/h.
b
Not to exceed 0.8–1.5 mEq/min.
682   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 6, November 2011
Hypomagnesemia is most commonly treated intravenously
because of the known GI intolerance of oral Mg1 (see
Table 5).
Hypermagnesemia. Hypermagnesemia (>2.5 mEq/L) may
be the result of excessive supplementation, renal disease,
laxative abuse, or increased intake of Mg-containing ant-
acids.1,3,27 Treatment for hypermagnesemia includes
dietary restriction, elimination of Mg-containing medica-
tions, and the use of diuretics and dialysis for severe cases
(see Table 5). In severe, symptomatic hypermagnesemia
(>12.5–32 mg/dL), 7.8–13.6 mEq of Ca over 5–10 min-
utes should be infused via central line.7 If volume status
allows, treatment may include provision of ½ NS with IV
furosemide to enhance urinary excretion of Mg.10
Ca
Ca is found mainly in bones and teeth. It is an extracel-
lular cation responsible for many physiological functions,
such as bone metabolism and neuromuscular function,
due to the protein-binding capacity of Ca. The intestine,
kidneys, and bones work synergistically to regulate Ca
balance in response to PTH levels and vitamin D status.
Vitamin D and PTH work in concert to maintain Ca
homeostasis. Ca levels target the parathyroid gland to
either increase or decrease production of PTH, which in
turn drives intestinal absorption of Ca, renal absorption/
excretion of phosphorus (P) and Ca, and bone mobiliza-
tion of Ca.30 PTH also converts the inactive form of vita-
min D to its active form (1,25-dihydroxyvitamin D;
calcitriol), to enhance Ca absorption in the GI tract.30 This
functionality is decreased in the setting of vitamin D defi-
ciency. Together, PTH and calcitriol activity targets the
proximal renal tubular cells to increase and/or decrease
Ca and P reabsorption.1,30 They are also responsible for
regulating the release of skeletal Ca into the ECF, in an
effort to augment the consequences of hypocalcemia.1
The assessment of Ca status must include an evalua-
tion of P and Mg status, in addition to PTH and vitamin
D status. Serum P and Ca have a reciprocal relationship,
whereby when one goes up the other comes down.3
Clinically, in cases of rapid correction of hypophos-
phatemia, the increased rate of Ca entering the cell can
lead to life-threatening hypocalcemia. Because of this
relationship, Ca and P levels need to be assessed prior to
establishing a treatment plan. Furthermore, hypomag-
nesemia is associated with hypocalcemia, which is likely
related to an inhibition of PTH in the setting of subopti-
mal Mg levels.29 With concomitant hypomagnesemia and
hypocalcemia, Mg must be corrected prior to achieve-
ment of a normalized Ca level.
The DRI of Mg for adults >18 years of age is 1,000–
1,200 mg/d28 and is approximated to be 10–15 mEq/d6 for
PN-dependent individuals, with adjustments as needed.
Oral supplementation is better absorbed when taken with
a meal to improve the solubility of the Ca salts. Na and
protein intake is proportionately related to Ca excretion in
the urine and ultimately to bone loss.31,32 Fortunately, the
P content of dietary protein augments this hypercalciuric
effect of proteins. Regardless of dietary content, absorp-
tion is dependent on adequate GI and renal function.
Hypocalcemia. Hypocalcemia can be defined in the pres-
ence of a normal albumin level, as a serum Ca <8.5 mg/
dL. Nearly 50% of serum Ca is protein bound, and there-
fore, in the presence of hypoalbuminemia, a corrected
Ca, or preferably ionized Ca, should be used10 (see Table
1). True hypocalcemia increases PTH production and
vitamin D activation in an effort to regain homeostasis.
Elevated PTH increases renal P excretion, mobilizes skel-
etal Ca, and enhances Ca absorption in the GI tract
through activation of vitamin D. Increased renal P excre-
tion results in decreased serum P levels, which drives the
extracellular movement of Ca.
Treatment of hypocalcemia depends on the Ca level
and the presence of symptoms (see Tables 3 and 4). If the
serum Ca level is >7.5 mg/dL and/or there is an absence
of symptoms, dietary intake should be optimized, and oral
supplementation should be considered (see Table 5).
Although true hypocalcemia is usually unrelated to die-
tary sources, this treatment option should be exhausted as
the first-line therapy. Symptoms begin to develop as levels
drop below 7.5 mg/dL. In these cases, IV supplementa-
tion is necessary. In the presence of hypomagnesemia or
hyperphosphatemia, Mg and P levels will need to be cor-
rected prior to the replacement of Ca.
Hypercalcemia. Hypercalcemia (>10.5 mg/dL) develops in
the setting of bone catabolism, resulting in an increased
movement of Ca into the ECF. This is precipitated by
immobilization, malignancies, and primary hyperparathy-
roidism, along with other factors.3 Elevated Ca concentra-
tions suppress PTH production, thus reducing concomitant
skeletal Ca loss, in the presence of rapid mobilization.
Hypercalemia targets the kidneys to excrete excess Ca into
the urine to prevent toxic levels in the serum.
Treatment is aimed at the underlying cause of the
increased bone mobilization of Ca stores. In addition to
this, after symptoms develop (see Tables 3 and 4) or serum
Ca levels exceed 12 mg/dL, acute treatments are needed
concomitantly (see Table 5). These treatments include
dietary restriction, fluid resuscitation, and a reduction of
Ca-containing medications. In the case of severe hyper-
calcemia (>15 mg/dL) rapidly infused NS increases renal
excretion of Ca. This, followed by administration of diu-
retics, can assist in normalizing serum Ca levels.6 Dialysis
may be required if the serum Ca levels do not respond to
the NS infusion to prevent calcifications.

P will require IV supplementation, as will also the patient
P is the primary intracellular anion responsible for cellu-
lar and bone structure, storage and transfer of energy in
the form of adenosine-triphosphate, and is an acid-base
buffer. Although P imbalances can occur in light of many
clinical scenarios, imbalances are typically a result of
altered intestinal absorption, renal insufficiency, bone
resorption/deposition, or cellular redistribution and are
highly regulated by endocrine function.
Intestinal absorption of P is dependent on serum P
levels and vitamin D status. The intestine can absorb up
to 80% of dietary intake in the presence of hypophos-
phatemia and/or elevated PTH. Within the kidney, the
glomerulus regulates P absorption in response to PTH,
acid-base imbalance, and volume expansion.1
Hyperparathyroidism is the main contributor to increased
urinary P loss and to mobilization of P from the Ca-P
pool, within the bone matrix. Lastly, intracellular shifts
can lead to P imbalance. Anabolism, acid-base imbal-
ances, and hormone secretions lead to intracellular shifts
depleting serum P. In clinical practice, this is most often
seen when a high carbohydrate load is administered, thus
providing PN with inadequate P content, and/or in cases
of refeeding syndrome. In refeeding syndrome, hypophos-
phatemia results because of the increased requirement
for the phosphorylation of glucose.18-20
The assessment of P status should include an evalu-
ation of Ca, PTH, and vitamin D status. As discussed
earlier, serum Ca and P have a reciprocal relationship, in
which an excess of one results in a depletion of the other.3
It is also clear that hypoparathyroidism leads to increased
renal absorption of P, whereas vitamin D deficiency leads
to decreased GI absorption.1 All 3 components are vital to
the overall assessment of P status.
The DRI for adults >18 years of age is 700 mg/d and
is approximated to be 20–40 mmol/d6 for PN-dependent
individuals, with adjustments as needed. Dietary P
absorption is reduced significantly in the presence of vita-
min D deficiency and with the use of P-binding antacids.
Whether supplemented by mouth or IV, absorption
depends on adequate GI and renal function.
Hypophosphatemia. Hypophosphatemia is defined as a
serum P level <2.7 mg/dL. Although serum P levels may
be depressed (below reference range), this is not a reflec-
tion of intracellular or total body stores of P. Since P
shifts between the intracellular and extracellular com-
partments, assessment must include all parameters out-
lined above to determine a treatment plan.
Asymptomatic mild hypophosphatemia (2.3–2.7 mg/
dL) can be treated with oral supplementation and increased
dietary intake, in most cases (see Tables 3–5). Symptomatic
patients with hypophosphatemia and/or moderate to severe
depletion (1.5–2.2 mg/dL and <1.5 mg/dL, respectively)
Fluid and Electrolyte Management / Rhoda et al   683
with intestinal failure6,25,33 (see Tables 3–5). P supplemen-
tation can be given orally or by IV and delivered as K or Na.
Potassium phosphate should be avoided when P levels
exceed 4 mmol/L, to reduce the development of hyper-
kalemia.6,17,25 If IV supplementation is indicated, infusions
should be over the course of 6 hours or more to prevent
rapid correction leading to rebound hypocalcemia (see
Table 5).
Hyperphosphatemia. Hyperphosphatemia is defined by an
elevation in serum P to >4.5 mg/dL. As with hypophos-
phatemia, elevated P levels do not reflect total body
stores. Assessment of P status requires an evaluation of
intestinal absorption, renal function, bone absorption/
deposition, and cellular redistribution to develop a thor-
ough treatment plan.
Treatment of asymptomatic hyperphosphatemia
starts with reducing the amount of P ingested and/or the
use of phosphate binders (see Tables 3–5). Phosphate
binders, such as aluminum-containing antacids, must be
monitored closely because of the potential for aluminum
toxicity. Symptomatic patients with hyperphosphatemia
may require volume resuscitation or dialysis in the setting
of dehydration and renal insufficiency. When the Ca-P
product exceeds 55 mg2/dL,33 there is a risk of forming
salt precipitants leading to soft-tissue calcifications. In
these cases, dialysis is also required to prevent vascular
calcifications.
Chloride and Bicarbonate
Chloride (Cl) and bicarbonate (HCO3−) are anions found
primarily in the ECF and used to regulate acid-base bal-
ance and osmotic pressure. Carbon dioxide (CO2) is regu-
lated by the lungs, and HCO3− (often reported as CO2) is
regulated by the kidneys. The pulmonary and renal sys-
tems maintain serum pH by adjusting excretion as devia-
tions in pH occur. The kidneys are the primary regulatory
mechanism for maintaining HCO3− and Cl levels, with
the proximal renal tubules being the site of reabsorption
and excretion.3
Serum CO2 and Cl abnormalities develop during
acid-base imbalances, in which the pulmonary and renal
systems attempt to compensate for pH shifts in an effort
to regain homeostasis. CO2 is a weak acid excreted by the
lungs. As the serum pH changes, the lungs adjust alveolar
ventilation in an effort to retain or excrete CO2, while the
kidneys retain or excrete hydrogen and HCO3−. Serum
CO2 is typically elevated during alkalosis and depressed
during acidosis, while Cl levels typically respond in the
opposite direction as CO2.
Adequate intake of Cl for PN-dependent individuals
is 2 g/d and approximately 1–2 mEq/kg of body weight,
684   Journal of Parenteral and Enteral Nutrition / Vol. 35, No. 6, November 2011
with adjustments made as needed. In PN, CO2 levels are
driven by the acetate dose, which varies based on the
acid-base balance. Absorption occurs in the small intes-
tine, as both Cl and HCO3− tend to follow Na for absorp-
tion.34 Although colonocytes have the ability to absorb
small amounts of Cl and HCO3−, this is likely more pro-
nounced in malabsorption syndromes, where the colon
compensates for decreased intestinal absorption.35,36
CO2 is a measure of total HCO3− in all the chemical
forms (dissolved CO2, carbonic acid, and bicarbonate).
Since carbonic acid and dissolved CO2 are negligible,
serum CO2 is an acceptable measure for assessing HCO3−.
Because Cl and HCO3− are both anions in the ECF, they
are inversely related in that as one increases the other
must decrease.3 This functionality is essential to main-
taining osmotic pressure.
During an acid-base imbalance, serum CO2 greatly
affects K balance, as K and CO2 also are inversely related.
An example of this is seen during metabolic acidosis,
where an elevated serum CO2 correlates with hypokale-
mia. The opposite is true of a metabolic alkalosis. Because
of the interrelationships between these electrolytes, a
thorough assessment includes evaluation of CO2, Cl, and
K.
When treating electrolyte abnormalities and/or pro-
viding IV hydration, assessing Cl and CO2 levels is imper-
ative for selecting the appropriate therapy. Medications
can worsen imbalances, as diuretics and H2 blockers con-
tribute to Cl wasting and antacids contain bicarbonate.6
With all Cl and CO2 imbalances, the workup should
include the assessment of medications. The first step is
treating the underlying condition, followed by assessing
all exogenous sources of Cl or bicarbonate. IV medica-
tions, IV hydration, and PN solutions often contain Cl
and/or bicarbonate, which can lead to an imbalance over
time. Maintenance fluids for hyperchloridemia and/or
depressed serum CO2 should be ½ NS, Lactated Ringers,
and/or dextrose in 5% water to improve the ratio of
Cl:CO2 in the ECF (see Table 2). Hypochloridemia and/
or elevated serum CO2 levels respond best to NS, to
improve the ratio of Cl:CO2. For PN-dependant patients,
an adjustment of the Cl and/or acetate content is needed
in the presence of abnormalities.
Conclusion
The intricacy of fluid and electrolyte management in
patients with complex intestinal failure can be challeng-
ing and the treatment multifactorial. Severe abnormali-
ties can be life threatening if the appropriate management
is not promptly instituted. Assessment involves a thor-
ough review of the underlying disease process, fluid sta-
tus, absorptive capacity of the GI tract, and renal function,
as treatment plans are adapted in response to these
parameters. One guideline will not fit every case, and
therefore a multispecialty milieu will enhance clinical
judgment and promote education, both critical compo-
nents of optimal patient outcome and clinician growth.
Glossary
  1. Osmolarity (lab calculated)*: number of solutes in
1 L of solution (mOsm/L)
  2. Osmolality (measured)*: concentration of body
fluids (ratio of solutes to water); the ability to cre-
ate oncotic pressure (mOsm/kg)
  3. Bone resorption: the process by which osteoclasts
break down bone and release the minerals (mainly
calcium), resulting in a transfer of calcium from
bone to the blood
  4. Tonicity: effective serum osmolarity; measure of
solutes that cause a shift of water from one com-
partment to another
  5. Isotonic: same tonicity as body fluids (280–300
mOsm/kg), example: 0.9% sodium chloride solution
  6. Hypotonic: tonicity < body fluids, example: 0.45%
sodium chloride solution
  7. Hypertonic: tonicity > body fluids, example: 3%
sodium chloride solution
  8. Reabsorption: absorption of already absorbed par-
ticles, usually referring to the kidneys
  9. Refeeding syndrome: elicited response after feeding
a severely malnourished catabolic patient; character-
ized by electrolyte abnormalities (ie, hypokalemia,
hypomagnesemia, hypophosphatemia); retention of
Na and water and possible depletion of thiamine
10. Hypovolemia: extracellular fluid deficit
11. Hypervolemia: extracellular fluid excess
*Differences between osmolality and osmolarity are quite
small, and the terms are often used interchangeably.
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