Fluids and Electrolytes
Donna Marie D. Abalajon, MD, FPCS, FPSGS
Introduction
• Changes in fluid volume and electrolyte composition
occur preoperatively, intraoperatively, and
postoperatively, as well as after trauma and sepsis.
Body Fluids
• Total Body Water (TBW)
• Water comprises 50-60% of total body weight
• The ratio between total body weight and TBW is
relatively constant per individual, and is a reflection of
body fat
• Gibbs – Donnan equilibrium equation
• The product of concentration of any pair of
diffusable cation and anion on one side of a
semi-permeable membrane will equal the
product of the same pair of ions on the other
side
• Osmotic Pressure
• The physiologic activity of electrolytes depends on:
• # of particles/unit vol (mmol/L)
• # of electric charges/unit vol (mEq/L)
• # of osmotically active ions/unit vol (mOsm/L)
• An equivalent of an ion = atomic weight (g) / valence
• mEq of cations must be balanced by the same number
of mEq of anions
• Osmotic pressure is measured in osm or mOsm (the
actual number of osmotically active particles)
• Osmotic Pressure
• Na, glucose, urea = the principal determinants of
osmolality
• Osmolality of IC and EC fluids is maintained b/w
290-310 mOsm
Body Fluid Changes
• Body fluid changes can be classified into:
• Disturbances in volume
• Disturbances in concentration
• Disturbances in composition
• Distubances in Volume
• A. Hypovolemia
• Most common fluid disorder in surgical patients
• Most common causes:
• Blood loss / hemorrhage
• GI losses:
• Vomiting, diarrhea, NGT suctioning, enterocutaneous
fistula
• Sequestration / Third spacing:
• From soft tissue injuries, burns, peritonitis, GI
obstruction, prolonged surgery
• Lab findings:
• Elevated BUN
• Urine osmolality > serum osmolality
• Decreased urine Na
System Volume Deficit Volume Excess
Generalized Weight loss Weight gain
Decreased skin turgor Peripheral edema
Cardiac Tachycardia Increased cardiac output
Hypotension/orthostasis Increased CVP
Collapsed neck veins Distended neck veins
Renal Oliguria ---
Azotemia
GI Ileus Bowel edema
Pulmonary --- Pulmonary edema
• Orthostatic hypotension
• also known as postural hypotension, head rush or a
dizzy spell
• sudden (less than 3 minutes) fall in blood pressure,
typically greater than 20/10 mm Hg
• occurs when a person assumes a standing position,
usually after a prolonged period of rest
• Collapsed neck veins
• Decreased skin turgor
• Oliguria and Anuria
• Oliguria and anuria are decreased or absent
production of urine, respectively.
• The decreased production of urine may be a sign of
dehydration, renal failure or urinary obstruction/urinary
retention.
• Azotemia
• abnormal levels of nitrogen-containing compounds,
such as urea, creatinine, various body waste
compounds, and other nitrogen-rich compounds in
the blood.
• Disturbances in Volume
• B. Hypervolemia / Volume excess
• Causes:
• Iatrogenic
• Secondary to renal dysfunction, CHF, cirrhosis
• Sx primarily CVS and pulmonary
• Elderly and px with cardiac disease may quickly develop
CHF in response to only moderate volume excess.
System Volume Deficit Volume Excess
Generalized Weight loss Weight gain
Decreased skin turgor Peripheral edema
Cardiac Tachycardia Increased cardiac output
Hypotension/orthostasis Increased CVP
Collapsed neck veins Distended neck veins
Renal Oliguria ---
Azotemia
GI Ileus Bowel edema
Pulmonary --- Pulmonary edema
• Bowel edema
• May be seen at the end of a long abdominal surgery
• Increases the intraabdominal pressure
• May have difficulty in abdominal closure
• Abdominal compartment syndrome
• Disturbances in Volume
• Volume control is by osmoreceptors and baroreceptors
that lead to return of plasma osmolality and volume to
normal.
• Disturbances in Concentration
• A. Hyponatremia
• Excess of EC water relative to sodium
• Usually a consequence of Na depletion or dilution
• EC volume can be high, low, or normal
• for hyponatremia in setting of hyperglycemia, we must
calculate corrected Na
• Hyponatremia
• Treatment:
• Most cases can be treated with WATER RESTRICTION.
• Na administration if severe.
• Hyponatremia can be asymptomatic until serum Na drops
below 20 mEq/L
• If with neurologic symptoms:
• Increase Na by no more than 1 mEq/L/hr until serum Na
reaches 130 mEq/L, or symptoms improve
• If asymptomatic
• Increase Na by no more than 0.5 mEq/L/hr to a maximum
increase of 12 mEq/L/day; slower for chromic hyponatremia
• Disturbances in Concentration
• B. Hypernatremia
• Either from loss of free water, or from gain of sodium in
excess of water
• Hypernatremia
Body System Signs and Symptoms
CNS Restlessness, lethargy, ataxia, irritability,
delirium, seizures, coma
Musculoskeletal Weakness
CVS Tachycardia, hypotension, syncope
Tissue Dry sticky mucous membranes, red swollen
tongue, decreased saliva and tears
Renal Oliguria
Metabolic Fever
• Classic hypovolemic hypernatremia: tachycardia,
orthostasis, hypotension
• Hypernatremia
• Treatment:
• Treat associated water deficit by replacing with
hypotonic fluid
• In hypovolemic patient, restore volume first before
addressing concentration abnormality
• For acute symptomatic hypernatremia: adjust rate to
decrease serum Na by no more than 1 mEq/hr, and 12
mEq/day
• For chronic hypernatremia, adjust rate to decrease serum Na
by no more than 0.7 mEq/hr
• Disturbances in Composition
• A. Potassium
• Normal serum K: 3.5 – 5.0 mEq/L
• Ave. daily K intake: 50 – 100 mEq/day; most excreted in
urine
• Only 2% of total body K is located in EC compartment,
but this amount is critical for cardiac and neuromuscular
function
• 1. Hyperkalemia
• Serum K > 5mEq/L
• Causes:
Hyperkalemia
Increased intake Potassium supplementation
Blood transfusions
Endogenous load/destruction: hemolysis,
rhabdomyolysis, crush injury, GI bleed
Increased release Acidosis
Rapid rise of EC osmolality
(hyperglycemia or mannitol)
Impaired excretion K-sparing diuretics
Renal insufficiency/failure
• 1. Hyperkalemia
• Signs and symptoms:
System Hyperkalemia
GI Nausea, vomiting, colic, diarrhea
Neuromuscular Weakness, paralysis, respiratory failure
Cardiovascular Arrhythmia, arrest
• ECG changes:
• Peaked T waves (early), widened QRS complex,
flattened P wave, prolonged PR interval, sine wave
formation, ventricular fibrillation
• 1. Hyperkalemia
• Treatment:
Goals
Reducing total body potassium
Kayexalate
oral: 15-30g in 50-100ml of 20% sorbitol
rectal: 50g in 200ml of 20% sorbitol
Dialysis
Shift K from EC IC
GI solution: Glucose 1 amp of D50 + regular insulin 5-10u IV
Bicarbonate 1 amp IV
Counteract cardiac effects
Ca gluconate 5-10ml of 10% solution
• 2. Hypokalemia
• Serum K < 3.5mEq/L
• More common in surgical patients
• Causes:
Hypokalemia
Inadequate intake Dietary
K-free IV fluids
K-deficient TPN
Excessive K Hyperaldosteronism
excretion Medications:
amphotericin,aminoglycosides, cisplatin,
ifosfamide
GI losses Direct loss of K from GI fluid (diarrhea)
Renal loss of K (gastric fluid from
vomiting or high NGT output)
• 2. Hypokalemia
• Signs and symptoms:
System Hyporkalemia
GI Ileus, constipation
Neuromuscular Decreased reflexes, fatigue, weakness,
paralysis
Cardiovascular Arrest
• ECG changes:
• U waves, T wave flattening, ST segment changes,
arrhythmias
• 2. Hypokalemia
• Treatment:
• Serum K < 4.0 mEq/L
• Asymptomatic, tolerating enteral nutrition: KCl 40
mEq per enteral access x 1 dose
• Asymptomatic, not tolerating enteral nutrition: KCl
20 mEq IV q2h x 2 doses
• Symptomatic: KCl 20 mEq IV q1h x 4 doses
• Recheck serum K 2h after end of infusion. If
<3.5mEq/L and asymptomatic, replace as per above
protocol
• Disturbances in Composition
• B. Calcium
• Less than 1% of total body Ca is located in EC
compartment
• 3 forms of Ca in serum: proteinbound (40%), complexed to
phosphates and other anions (10%), ionized (50%)
• Total serum Ca decreases by 0.8mg/dl for every 1g/dl
decrease in albumin
• Acidosis will decrease protein binding more ionized
Ca
• Normal serum Ca: 8.5 – 10.5 mEq/L (total)
• 4.2 – 4.8 mg/dl (ionized)
• Ave. daily Ca intake: 1-3 g/day; most excreted in feces
• 1. Hypercalcemia
• Most commonly due to primary hyperparathyroidism and malignancy
• Signs and symptoms:
System Hypercalcemia
GI Anorexia, nausea, vomiting, abdominal
pain
Neuromuscular Weakness, confusion, coma, bone pain
Cardiovascular Hypertension, arrhythmia
Renal Polyuria, polydipsia
• ECG changes:
• Shortened QT interval, prolonged PR and QRS segments,
increased QRS voltage, T wave flattening and widening, AV
block
• 1. Hypercalcemia
• Treatment:
• Treatment required when symptomatic, usually when
serum Ca reaches over 15mg/dl
• Replenish the associated water deficit, then induce brisk
diuresis with normal saline.
• 2. Hypocalcemia
• Causes:
• Pancreatitis, massive ST infections, renal failure, bowel
fistulas, hypoparathyroidism, toxic shock syndrome,
tumor lysis syndrome, abnormalities in Mg levels,
transient hypocalcemia after removal of a parathyroid
adenoma, massive blood transfusion
• Rarely results from decreased intake
• 2. Hypocalcemia
• Asymptomatic hypocalcemia may occur when hypoproteinemia leads to a
normal ionized Ca level
• Generally, symptoms do not occur until ionized Ca < 2.5 mg/dl
• Signs and symptoms:
System Hypercalcemia
Neuromuscular Hyperactive reflexes, paresthesias,
carpopedal spasm, seizures
Cardiovascular Heart failure
• Chvostek’s sign – spasm from tapping over facial nerve
• Trousseau’s sign – spasm from pressure to nerves and vessels of upper
extremity with a blood pressure cuff
• ECG changes:
• Prolonged QT interval, T wave inversion, heart block, atrial fibrillation
• 2. Hypocalcemia
• Treatment:
• Normalized ca level < 4.0 mg/dl:
• With gastric access and tolerating enteral nutrition: Ca
carbonate suspension 1250mg/5ml q6 per gastric access,
recheck ionized Ca level in 3 days
• Without gastric access or not tolerating enteral nutrition:
Ca gluconate 2g IV over 1 hour x 1 dose, recheck
ionized Ca level in 3 days
• If asymptomatic, can treat with oral or IV
• For acute symptomatic, give 10% Ca gluc IV to reach 7-9
mg/dl
• Must also correct associated deficits in Mg, K and pH
• Routine Ca supplementation is no longer recommended after
massive blood transfusion
• Disturbances in Composition
• C. Phosphorus
• Primary IC divalent anion
• Abundant in metabolically active cells
• Involved in energy production during glycolysis, also
found in high energy products like ATP
• 1. Hyperphosphatemia
• Causes:
Hyperphosphatemia
Decreased urinary Hypoparathyroidism
excretion hyperthyroidism
Increased PO4 intake IV hyperalimentation solutions
PO4 containing laxatives
Endogenous Rhabdomyolysis
mobilization of PO4 Tumor lysis syndrome
Hemolysis
Sepsis
Severe hypothermia
Malignant hyperthermia
• 1. Hyperphosphatemia
• Most cases are asymptomatic
• Chronic hyperphosphatemia can have metastatic deposition
of soft tissue Ca-P complexes
• Treatment:
• Phosphate binders like sucralfate or Al-containing
antacids
• Ca acetate tablets – useful when with assoc
hypocalcemia
• Dialysis for patients with renal failure
• 2. Hypophosphatemia
• Causes:
Hypophosphatemia
Decreased PO4 Malabsorption
intake Administration of phosphate binders
Decreased dietary intake from
malnutrition
IC shift of PO4 Respiratory alkalosis
Insulin therapy
Refeeding syndrome
Hungry bone syndrome
Increase in PO4
excretion
• 2. Hypophosphatemia
• Most cases are asymptomatic until with significant fall
• Treatment:
• Phosphate level 1.0 – 2.5 mg/dl:
• Tolerating enteral nutrition: Neutra-Phos 2 packets q6
per gastric tube or feeding tube
• No enteral nutrition: KPHO4 or NaPO4 0.15 mmol/kg
IV over 6h x 1 dose
• Recheck phosphate level in 3 days
• Phosphate level <1.0 mg/dl:
• Tolerating enteral nutrition: KPHO4 or NaPO4
0.25mmol/kg over 6h x 1 dose
• Recheck PO4 level after 4h after end of infusion; if
<2.5mg/dl, begin Neutra-Phos 2 packets q6h
• Not tolerating enteral nutrition: KPHO4 or NaPO4
0.25mmol/kg (LBW) over 6h x 1dose; recheck PO4
level 4h after end of infusion; if <2.5mg/dl, then KPHO4
or NaPO4 0.15mmol/kg IV over 6h x 1 dose
• Disturbances in Composition
• D. Magnesium
• Found primarily in intracellular compartment
• Normal dietary intake: 20 mEq/d; excreted in stool and
urine
• ½ of total body Mg is in bone
• 1/3 of remaining is bound to albumin
• In presence of hypoalbuminemia, plasma level of Mg may
be a poor indicator of total body stores
• 1. Hypermagnesemia
• Rare
• Causes:
• Severe renal insufficiency, Mg-containing laxatives and
antacids, excess intake, massive trauma, thermal injury,
severe acidosis
• 1. Hypermagnesemia
• Signs and symptoms:
System Hypermagnesemia
GI Nausea, vomiting
Neuromuscular Weakness, lethargy, decreased reflexes
Cardiovascular Hypotension, arrest
• ECG changes:
• Similar to hyperkalemia
• Increased PR interval, widened QRS complex, elevated
T waves
• 1. Hypermagnesemia
• Treatment:
• Eliminate exogenous sources of Mg
• Correct concurrent volume deficits
• Correct acidosis if present
• For acute symptomatic hyperMg: 5-10ml CaCl to
immediately counteract cardiovascular effects
• Dialysis if severe / persistent
• 2. Hypomagnesemia
• Causes:
Hypomagnesemia
Decreased Mg intake Starvation
Alcoholism
Prolonged IV fluid therapy
TPN with inadequate Mg
Increased renal Alcohol abuse
excretion Diuretic use
Administration of amphotericin B
Primary aldosteronism
GI losses Diarrhea
Malabsorption
Acute pancreatitis
• 2. Hypomagnesemia
• Signs and symptoms:
System Hypermagnesemia
Neuromuscular Hyperactive reflexes, muscle tremors,
tetany, seizures
Cardiovascular Arrhythmia
• ECG changes:
• Prolonged QT and PR interval, ST depression, flattening
or inverted P waves, torsades de pointes, arrhythmias
• 2. Hypomagnesemia
• Treatment:
• Mg level 1.0 – 1.8 mEq/L:
• MgSO4 0.5mEq/kg in 250ml normal saline IV
infusion over 24h x 3 days
• Recheck Mg level in 3 days
• Mg level <1.0 mEq/L:
• MgSO4 1mEq/kg in 250ml normal saline IV
infusion over 24h x 1day, then 0.5mEq/kg in 250ml
normal saline IV infusion over 24h x 2days
• Recheck Mg level in 3 days
• If pt has gastric access and needs a bowel regimen:
• Milk of magnesia 15ml (approx 49 mEq of Mg)
q24h per gastric tube; hold for diarrhea
Acid-Base Balance
• Body pH is maintained within a narrow range
(7.35-7.45) despite renal generation of large amounts
of HCO3 and normally large acid load as by-product of
metabolism
• Acid load is neutralized by buffer systems and excreted
by lungs and kidneys.
• Metabolic derangements respiratory compensation
• Respiratory derangements metabolic compensation
• Metabolic derangements respiratory compensation
• Mediated by chemoreceptors in brainstem and carotid body
• Acidosis – chemoreceptors – increase ventilation
• Alkalosis – decreased chemoreceptor activity – decrease
ventilation
• Respiratory derangements metabolic compensation
• Kidneys compensate by increasing or decreasing HCO3
reabsorption
• Acute – before renal compensation
• Chronic – after renal compensation
• A. Metabolic Acidosis
• Causes: Increased intake of acids, increased generation of
acids, increased loss of HCO3
• Body responds by: producing buffers, increasing ventilation
(Kussmaul’s respirations), increasing renal reabsorption and
generation of HCO3
• Must first determine anion gap (index of unmeasured anions)
• AG = Na – [Cl + HCO] in mmol/L
• AG <12 normal AG
• AG >12 high AG
• Adjust AG for albumin
• Corrected AG = actual AG – [2.5 (4.5 – albumin)]
• A. Metabolic Acidosis
• High anion gap metabolic acidosis
• Treatment:
• Volume resuscitation to restore perfusion, rather than
giving exogenous HCO3 to try to correct pH
• A. Metabolic Acidosis
• Normal anion gap metabolic acidosis
• The loss of HCO3 is accompanied by gain of chloride:
unchanged AG
• B. Metabolic Alkalosis
• Normally does not happen unless both increase in HCO3
generation and impaired excretion of HCO3 occur
• Worsened by K depletion
• Majority of px will also have hypokalemia
• Hypochloremic hypokalemic metabolic alkalosis can occur
in duodenal ulcer dse or pyloric stenosis
• Treatment:
• Replacement of volume deficit
• K replacement
• C. Respiratory Acidosis
• Retention of CO2 due to
decreased alveolar
ventilation
• Treatment:
• Treatment of underlying
cause
• Ensure adequate
ventilation
• May require intubation or
use of BIPAP
• C. Respiratory Alkalosis
• Due to alveolar
hypoventilation
• Treatment:
• Treatment of underlying
cause
• Controlled ventilation
may be required
Fluid Therapy
• The type of fluid administered depends on the patient’s
volume status and type of concentration or
compositional abnormality present.
• Alternative Fluids
• Hypertonic saline
• 3.5%, 5% - used for correction of severe Na deficits
• 7.5% - used for px with closed head injuries
• Colloids
• Used as volume expanders because they are confined to
intravascular space
• a. albumin
• b. dextrans
• c. hydroxyethyl starch
• d. gelatins
• Preoperative Fluid Therapy
• Eg. For a 55-kg female, how much maintenance fluid
should you give?
• Preoperative Fluid Therapy
• Preoperative evaluation of patient’s volume status and
preexisting electrolyte abnormalities
• Consider volume deficit in patients with:
• Obvious GI losses, poor oral intake, third-space losses
• Check for: tachycardia, orthostasis, oliguria,
hemoconcentration
• With cardiovascular signs of volume deficit: give 1-2 L
of isotonic fluid as bolus, followed by a continuous
infusion
• Monitor for signs of reversal of volume deficit:
• Acceptable vital signs
• Adequate urine output (0.5 – 1 ml/kg/hr)
• Correction of base deficit
• If with symptomatic electrolyte abnormality: correct first
until at least asymptomatic before proceeding with
surgery
• Intraoperative Fluid Therapy
• Upon induction of anesthesia, normal compensatory
mechanisms are lost.
• Monitor and replace:
• Blood loss
• Continued extracellular losses (eg. Bowel wall edema,
peritoneal fluid, wound edema)
• 500 – 1000 ml/hr of isotonic salt solution to replace ECF
losses
• Postoperative Fluid Therapy
• Daily assessment of current volume status and projected
ongoing losses.
• Correct any deficits from preop and intraop periods.
• Replace measured losses and insensible losses with
appropriate solutions.
• Resuscitation adequate if:
> acceptable vital signs
> adequate urine output
> correction of base deficit
• Thank you.
