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