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Fluids and Electrolytes
Presley Regional Trauma Center
Department of Surgery
University of Tennessee Health Science Center
Memphis, Tennessee
Body Fluid Compartments
• Approximates 60% of total body weight
• Composed of the intracellular and
extracellular compartments
• The intracellular compartment or
intracellular volume (ICV) constitutes 40%
of total body weight
• Extracellular volume (ECV) makes up the
remaining 20%
Total Body Water
• Composed of interstitial fluid (IF) and the
intravascular or plasma volume (PV)
• The PV constitutes 25% of ECV (5% of
total body weight) – remainder is IF
• Red cell volume, approximately 2 to 3% of
TBW, is part of the ICV
• Total blood volume is approximately 7 to
8% of total body weight
ECV
• Sufficient water is required to replace
obligatory GU losses of approximately
1L/day and GI losses of 100 - 200ml/day
• Insensible water losses must also be
considered in estimating maintenance fluid
- Amount to 8 to 12ml/kg/day
- Equally divided into respiratory and
cutaneous water loss
- Cutaneous losses increase by 10% for each
degree of temperature greater than 37°C
Requirements
• Daily sodium intake approaches 100 to
250mEq/day
• Balanced by sodium losses in sweat, stool,
and urine
• Renal conservation of sodium is
extraordinary
• In cases of profound volume depletion,
urinary losses of sodium may be less than
1mEq/day
Electrolytes
• In the perioperative period, adequate
maintenance of sodium may be achieved
with an intake of 1 to 2mEq/kg/day
• Normal potassium intake is approximately 40
to 120mEq/day
• 10-15% is excreted as normal urinary losses
• With normal renal function, body potassium
stores can be maintained with an intake of
approximately 0.5 to 1.0mEq/kg/day
Electrolytes
Perioperative Fluid Requirements
• Appropriate management of fluids and
electrolytes in the perioperative period
requires a flexible yet systematic approach
• Ensures that fluid administration is
appropriately tailored to the patient's
changing requirements
Perioperative
• The amount of fluids administered in the
immediate post-op period must take into
account the existing deficit, maintenance
requirements, and any ongoing losses
• Estimation of the existing deficit must
incorporate an approximation of intra-op
blood loss as well as fluid losses from
evaporative and third-space fluid
sequestration
Perioperative
• Extravascular fluid sequestration represents
an important source of intra-op fluid loss
• Extensive dissection at the operative site
induces a localized capillary leak, resulting
in extravasation of intravascular fluid into the
interstitium with edema formation
• The loss of intravascular volume via this
route depends on the extent of exposure
and degree of dissection
Losses
• For example, estimated intravascular fluid
losses associated with IHR are 4ml/kg/h,
while losses during AAA repair may be as
high as 8ml/kg/h
• This capillary leak may persist as long as
24h into the post-op period and should be
considered as part of ongoing losses in the
immediate post-op period
Losses
• GI losses (stomas, tubes/drains, or fistulae)
comprise ongoing fluid losses
• These losses may be accurately estimated
by closely following recorded hourly outputs
• The electrolyte composition of the output
depends on the source of effluent
• Replacement fluids should be chosen to
best approximate the composition of the
ongoing losses
Losses
• Post-op fluid orders should take into
account the overall fluid balance in the OR
as an estimate of the existing deficit along
with maintenance fluid requirements and
any ongoing losses
• The preferred approach is to reassess the
patient frequently to determine volume
status
Post-op
• Evaluation of heart rate, blood pressure,
and most importantly, hourly urine output
provides an excellent measure of
intravascular volume status
• Orders for IVF should be rewritten
frequently to maintain a normal heart rate,
a urine output of approximately 1ml/kg/h,
and adequate blood pressure
Post-op
Disorders of Sodium Homeostasis
• Maintenance of a normal serum [sodium] is
intimately associated with control of plasma
osmolarity
• Posm= 2×Plasma [Na+] + [Gluc]/20 +
[BUN]/3
• Plasma [Na+] alone provides no information
about the total content of sodium in the body
but simply provides an estimate of the
relative amounts of free water and sodium
Sodium
• Maintenance of the plasma osmolarity within
normal limits depends on the ability of the
kidneys to excrete water, thus preventing
hypoosmolarity, and on a normal thirst
mechanism with access to water to prevent
hypernatremia
• The ability to excrete maximally dilute urine
(<100mOsm/kg) allows the kidneys to
excrete in excess of 18L of water per day
Osmolarity
• In the presence of normal renal perfusion
and intact renal function, ADH is the
principal regulator of serum osmolarity
• 1-2% reduction in Posm maximally inhibits
ADH release – maximally dilute urine
• 1-2% increase in Posm or a 5-10% decrease
in blood volume or pressure stimulates ADH
• With both a low Posm and blood volume or
pressure, the latter effect will dominate
Osmolarity
• Begins with an assessment of the serum
osmolarity
• if serum osmolarity is high, then it is
important to consider the possibility of other
effective plasma osmoles
• Hyperglycemia shifts H2O from cells, leading
to dilutional hyponatremia – f or every
100mg/dl rise in glucose the [Na+] falls by
1.3mEq/l
Hyponatremia
• In rare cases, the serum osmolarity may be
normal
• This phenomenon is referred to as
pseudohyponatremia and is caused by
hyperlipidemia or hyperproteinemia
• It is an artifact of the laboratory assay
Pseudohyponatremia
• More frequently, a low [Na+] will be
associated with reduced plasma osmolarity
• The etiology and treatment of hypoosmolar
hyponatremia may be classified into 3
groups depending on the ECV status of the
patient
Hyponatremia
• Most common causes are Na+ loss
• A reduction in ECV leads to an increase in
ADH secretion, impairing the kidney's ability
to excrete free water
• Either administration of Na+-free solutions or
the ingestion of free water induced by thirst
aggravates the resulting hyponatremia
Hypovolemic Hyponatremia
• Typically, perioperative isotonic losses
(plasma, gastric losses) are replaced with
hypotonic solutions in the face of mild
hypovolemia
• Treatment involves replenishing the
extravascular volume with isotonic fluids in
concert with restriction of free water
Hypovolemic Hyponatremia
• Hyponatremia in the presence of an
increased extravascular volume
• Represents the next most common scenario
in the perioperative period
• Edematous states in which there is a
reduction in the effective circulating volume
• Low CO states, cirrhosis, and other
hypoalbuminemic states are the more
common etiologies
Hypervolemic Hyponatremia
• Both water restriction and Na+ restriction are
necessary
• Depending on the severity of the
hyponatremia, a loop diuretic may be
required to increase both Na+ and water loss
• In most cases, this induces an excess of
urinary water loss over Na+ loss and should
correct the hyponatremia
Hypervolemic Hyponatremia
• Patients with a normal ECV status and
hypoosmolar hyponatremia
• SIADH
• Nausea, pain, and narcotics, all of which are
common in the post-op period, may result in
SIADH and contribute to post-op
hyponatremia
Euvolemic Hyponatremia
• Diagnosis is confirmed by demonstrating a
low plasma osmolarity, a less than
maximally dilute urine (Uosm. > 100mOsm/l),
and renal salt wasting (UNa. > 20mEq/l)
• Treatment includes management of the
underlying cause and water restriction
• Isotonic (0.9%) saline should not be
administered to patients with SIADH as it
may cause the plasma [Na+] to fall
SIADH
• The presence of Sx depends on the rate at
which hyponatremia occurred
• Sx of increased ICP from cerebral edema
are the most prominent features and may be
present at plasma [Na+] < 125mEq/l if the
development of hyponatremia was rapid
• If the reduction in [Na+] occurs slowly, then
symptoms may not be evident until plasma
[Na+] drops to as low as 110mEq/l
•
Treatment
• Too rapid correction may result in CPM
• If the patient is aSx or mildly symptomatic,
then the goal should be to raise the [Na+] by
approximately 0.5mEq/h
• If the patient is Sx with coma or convulsions,
then more rapid correction is necessary
• Goal is to administer sufficient Na+ until
either the symptoms have improved or the
plasma [Na+] has increased by 5mEq/l
Treatment
• The following formula may be used to
estimate the amount of Na+ required to raise
the [Na+] to a safe level (approximately
120mEq/l)
- Na+ deficit = 0.60 × Lean body weight (kg) ×(120 - Measured plasma Na+)
Treatment
• Far less common than is hyponatremia
• Cellular shrinkage caused by fluid shifts
from the intracellular space to the
extracellular compartment may cause
confusion, coma, and intracranial
hemorrhage
• Symptoms are usually not evident below a
plasma [Na+] of 160mEq/l
Hypernatremia
• Occurs as a result of excessive free HOH
loss
• Frequently associated with hypovolemia
• Excessive insensible losses caused by
fever, hyperventilation, and burns or
hypotonic fluid losses due to perspiration or
severe diarrhea are the principal causes
Hypernatremia
• If hypovolemia is sufficiently severe that
tissue perfusion is compromised, then initial
therapy should be isotonic saline until tissue
perfusion is restored
• If perfusion is adequate, then 0.5 NS or
D5W is sufficient to return plasma [Na+] to
normal
Treatment
• Rapid correction of severe hypernatremia
may cause irreversible neurological deficits
- Should not be corrected at a rate faster than
0.5 to 1.0mEq/l per hour
• In the presence of Sx, free water should be
administered either to return the plasma
[Na] to that documented before the Sx or to
reduce the [Na] by about 6mmol/l
- Water deficit = TBW × {(Plasma [Na] ÷Desired plasma [Na]) - 1}
Treatment
Disorders of Potassium
Homeostasis
• The major intracellular cation
• Only 2% is located in the extracellular fluid
• Slight alterations in plasma [K+] may have
dramatic effects on muscle contraction and
nerve conduction as the [gradient] across
the plasma membrane is the main
determinant of membrane excitability
• Abnormalities in plasma [K+] should be
treated expeditiously
Potassium
• Usually from GI, kidney or skin losses
• Cardiac arrhythmias – exacerbated with
metabolic alkalosis, dig or hypercalcemia
• ECG = T-wave flattening or inversion and
depressed ST segments, followed by U
waves and a prolonged QT interval
• Replacement should be geared toward rapid
correction of plasma [K+], followed by slower
repletion of the total body K+ deficit
Hypokalemia
• Main risks are weakness and myocardial
irritability
• ECG = increase in T-wave amplitude,
leading to a narrow, peaked symmetrical T
wave, followed by reduced P-waves and
widening of the QRS
• If untreated, may eventually cause a
sinusoidal ECG complex and ultimately
ventricular fibrillation
Hyperkalemia
Disorders of Mineral Homeostasis
• Total body stores are approximately 1000g
• Almost 99% is in bone
• The remainder is located within the ECF
• Either free (40%) or bound to albumin (50%)
or other anions such as citrate, lactate, and
sulfate
• Only the free or ionized component is
biologically active
Calcium
• Acid-base alterations affect the binding of
calcium to albumin
• Similarly, changes in serum protein levels
affect total serum calcium
• The ionized calcium level can be estimated
using the following formula
- Ionized calcium (mg/dl) = Total serum calcium
(mg/dl) - 0.83 × Serum albumin (mg/dl)
Calcium
• Most frequent cause = low serum albumin
• In this case, the ionized fraction remains
normal, and no treatment is indicated
• Other causes include acute pancreatitis,
massive soft tissue infection, small-bowel
fistulae, hypoparathyroidism and massive
blood transfusion
Hypocalcemia
• Earliest Sx include numbness or tingling in
the circumoral region or at the tips of the
fingers
• Tetany or seizures may arise at more
profound levels
• A positive Trousseau's sign or Chvostek's
sign may be suggestive of it
• Alters myocardial repolarization and results
in a prolonged QT interval
Hypocalcemia
• Primary hyperparathyroidism and malignant
disease account for 90% of cases
• Sx include confusion, lethargy, coma,
muscle weakness, anorexia, nausea,
vomiting, pancreatitis, constipation, renal
stones, nephrogenic DI and polyuria
• ECG = shortened QT interval
Hypercalcemia
• The principal intracellular divalent cation
• Approximately 50% of total body
magnesium is found in bone and is not
readily exchangeable
• Absorption occurs throughout the small
intestine and is reabsorbed effectively in the
renal tubules
Magnesium
• May occur because of poor nutritional
intake, malabsorption, or increased renal
excretion
• Characterized by neuromuscular and CNS
irritability
• Low serum magnesium levels appear to
impair PTH excretion and may induce
hypocalcemia refractory to calcium
supplementation unless corrected
Hypomagnesemia
• The most abundant intracellular anion
• Only 0.1% of total body phosphorus is in the
extracellular fluid compartment
• As a result, circulating plasma levels do not
reflect total body stores
Phosphate
• May occur as the result of impaired
intestinal absorption or increased renal
excretion
• Hyperparathyroidism may induce a drop in
serum phosphate levels through an increase
in renal excretion
• Careful monitoring of phosphate should also
occur with the administration of parenteral
nutrition after prolonged starvation because
profound hypophosphatemia may result
Hypophosphatemia
• Most commonly seen in the setting of
impaired renal phosphate excretion
• In this scenario is frequently associated
with hypocalcemia.
• Similarly, hypoparathyroidism reduces
renal phosphate excretion, leading to an
increase in serum phosphate levels
Hyperphosphatemia
Acid-Base Abnormalities
• Arises as a result of retention (or
administration) of fixed acids or the loss of
bicarbonate
• Categorized by the presence or absence of
an anion gap (AG)
- Addition of fixed acids results in an AG
metabolic acidosis
- Bicarbonate loss results in a nonAG metabolic
acidosis
Metabolic Acidosis
• Characterized by an elevated plasma [HCO3-]
• May occur as a result of one of three
mechanisms
- Loss of acid from the GI tract or urine
- Administration of HCO3-or a precursor, such as
citrate (as occurs following massive blood
transfusions)
- Loss of fluid with a high chloride/bicarb ratio
Metabolic Alkalosis
• Either chloride sensitive or chloride resistant
to the extent that they are reversed by the
administration of NS
• Treatment should be directed toward the
underlying cause
Classification
• Surgical patients undergo acute alterations
in the volume and composition of fluids in
the intracellular and extracellular spaces
• To a great extent, these changes occur as a
result of the patient's underlying disease
• These alterations are not limited to patients
requiring urgent operative intervention
Summary
• Elective surgery may result in dramatic fluid
shifts without significant blood loss
• In addition to changes in fluid volume,
surgical patients may develop potentially
dangerous fluctuations in concentrations
and total body content of important lytes
• Precise peri-op management of fluids and
electrolytes is required to minimize peri-op
morbidity and mortality
Summary