Fluid and Electrolyte Management

of the Surgical Patient

Introduction
Changes in both fluid volume and electrolyte
composition occur preoperatively, intraoperative, and
postoperatively, as well as in response to trauma and sepsis.
 BODY FLUIDS

 Total BodyWater constitutes approximately 50% to 60%

of total body weight
Three functional fluid compartments
1. Intracellular water(40%)— (2/3).
2. Extracellular water(20%)—(1/3).
 Plasma (5%)-(1/4) .
 Interstitial fluid(15%)
 Composition of Fluid Compartments

The ECF compartment is balanced between the principal cation-

Na+, and the principal anions- Cl- and HCO3-.

The ICF compartment is comprised primarily of the cations, K+,

Mg++, and of the anions, PO4-2 , sulphates and proteins.

The concentration gradient between compartments is maintained

by Na+-K+ ATPase

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Composition of Fluid Compartments

Chemical composition of
body fluid compartments.
 Movement of ions and proteins between the various fluid

compartments is restricted, but water is freely diffusible.

 Sodium is confined to the extracellular fluid compartment, and

because of its osmotic and electrical properties, it remains

associated with water.
 Osmotic Pressure

 The movement of water across a cell membrane depends

primarily upon osmosis across a semipermeable membrane.

 The principal determinants of osmolality are the concentrations of

sodium, glucose, and urea (blood urea nitrogen [BUN]):

 Calculated serum osmolality = 2 sodium + (glucose/18) +

(BUN/2.8
 Body Fluid Changes

Disorders in fluid balance may be classified into three

general categories:
 Volume disturbances
 Concentration disturbances
 Composition disturbances
may occur simultaneously
 1.Disturbances in Fluid Balance

Extracellular volume deficit is the most common fluid

disorder in surgical patients
Can be
 Acute volume deficit - deficit is associated with
cardiovascular and central nervous system signs
 Chronic deficits -display tissue signs,such as a decrease
in skin turgor and sunken eyes, in addition
to cvs and CNS sign
 Urine osmolality usually will be higher than serum
osmolality, and urine sodium will be low, typically<20
mEq/L.
 Serum sodium concentration does not necessar-
ily reflect volume status and therefore may be high,
normal,or low when a volume deficit is present.
Causes of volume deficit in surgical patients
 loss of GI fluids from nasogastric suction, vomiting,
diarrhea, or enterocutaneous fistula
 sequestration secondary to soft tissue injuries, burns,
 Intra-abdominal processes such as peritonitis,obstruction,
or prolonged surgery can also lead to massive volume
deficits.
 Extracellular volume excess may be iatrogenic or
secondary to renal dysfunction, congestive heart failure,
or cirrhosis.
 Treatments

Fluid volume deficit Replacement

• Blood loss: RL, NS, Blood
• Extra cellular fluid: RL, NS
Rate
• fast until the vital signs are corrected and adequate urine output
• 1-2 liter over 30 minutes to one hour
Monitoring
• general condition & vital signs
• urine out put - hourly
• chest –overload- esp. in children & elderly
 Fluid volume excess

• Stop IV fluids (Fluid restriction)

• Diuretics: e.g. Furosemide

 2.Volume Control
osmoreceptors and baroreceptors.
 blood volume:
Osmolality > BP: Baroreceptor
310 atrial stretch
activation
mosmoles receptor
Osmoreceptors
Neural connection to Neural connection
in hypothalamus
hypothalamus to hypothalamus

AVP synthesised in
hypothalamus and released
from post pituitary

AVP activates collecting

duct
epithelium

Aquaporins inserted into

apical membranes

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↑ water resorption
 3.Concentration Changes

 Sodium
 Normal range is 135-145 mEq/L
 Hyponatremia
• when there is an excess of extracellularwater relative to sodium.
• As consequence of either sodium depletion
or dilution.
Post-op patients are particularly prone to increased
secretion of antidiuretic hormone (ADH),
• Drugs can cause water retention and subsequent
hyponatremia, such as
 antipsychotics
antitricyclic antidepressants
ACEI.
Depletional causes of hyponatremia are associated with
 Decreased sodium intake
 Increased loss of sodium-containing fluids :
• GI loss( vomiting, prolonged nasogastric suctioning,
or diarrhea; and
• renal losses due to diuretic use or primary renal
disease.
 Pseudo hyponatremia
Hyponatremia also can be seen untreated hyperglycemia
or mannitol administration.
When hyponatremia in the presence of hyperglycemia is
being evaluated, the corrected sodium concentration
should be calculated as for every 100-mg/dL increment in
plasma glucose above normal, the plasma sodium should
decrease by 1.6 mEq/L
Clinical features
 Principles of management for Hyponatremia

 Delayed/inadequate treatment leads to brain edema /

herniation/death.
 Too rapid correction may lead to cerebral ischemia, damage

to BBB or osmotic demyelination syndrome.

 Free water restriction.

 Administration of sodium(3% normal

saline/hypertonic solutions)
 Hypernatremia

From loss of free water or gain of sodium in excess of water.

Hypervolemic hypernatremia due to
 Administration of sodium-containing fluids,(sodium
bicarbonate,
 mineralocorticoid excess as seen in hyperaldosteronism,
Cushing’s syndrome,congenital adrenal hyperplasia.
 Normovolemic hypernatremia due to
 Renal causes-diabetes insipidus, diuretic use, and
renal disease,
 Non renal causes -water loss from the GI tract or
skin, although the same conditions can result in
hypovolemic hypernatremia.
 although the same conditions can result in
hypovolemic hypernatremia.
Hypovolemia hypernatremia due to
 the urine sodium concentration is <20 mEq/L and urine
osmolarity is <300 to 400 mOsm/L.
 diarrhea,fever,
 via tracheotomies during hyperventilation.
 Symptoms are rare until the serum sodium
concentration exceeds 160 mEq/L
Treatment of Hypernatremia
 Composition Changes

1.Potassium Abnormalities
Hyperkalemia
 serum potassium concentration above the normal range
of 3.5 to 5.0 mEq/L.
 Increased intake (oral or IV supplementation)
 Hemolysis, rhabdomyolysis, and crush injuries (ICF-ECF
 potassium-sparing diuretics, ACEinhibitors, by interfere
with aldosterone activity, inhibiting the normal renal
mechanism of potassium excretion.
Hypokalemia-common in surgical patient
below 3.5 mEq/L
 Inadequate intake
Dietary, potassium-free intravenous fluids, potassium-
deficient TPN
 Excessive potassium excretion
Hyperaldosteronism
Medications –Amp b,cisplatin
 GI losses
Direct loss of potassium from GI fluid (diarrhea)
Renal loss of potassium (to conserve sodium in response
to gastric losses
 Clinical manifestations

Hyperkalemia Hypokalemia
 Treatment approach to hyperkalemic

 Intravenous calcium to antagonize the membrane actions

of hyperkalemia
Calcium gluconate 10ml of 10% over 2-3 min.
 Intravenous insulin (50ml of 50 %DW +10IU RI) to drive
extracellular potassium into cells
 loop or thiazide diuretics if renal function is not severely
impaired, and/or dialysis if renal function is severely
impaired)
Treatment approach to hypokalemia
2.Calcium Abnormalities
Daily calcium intake is 1 to 3 g/d
Majority within the bone matrix, with <1% found in the ECF
Hypercalcemia - a serum calcium level above the normal range of 8.5
to 10.5 mEq/L
Cause
• Primary hyperparathyroidism
• malignancy(bony metastasis
• Excessive ingestion of calcium or vitamin D
• Immobilization – causes bone loss
Hypocalcemia
 serum calcium level below 8.5 mEq/L
Causes
 pancreatitis, massive soft tissue infections such as
necrotizing fasciitis,
 renal failure,hypoparathyroidism,
 Malignancies(breast and prostate cancer by increased
bone formation.
 Massiveblood transfusion with citrate binding is
Clinical manifestations

Hypercalcemia
Hypocalcemia
 Treatments of hypercalcemia

Mild hypercalcemia -calcium <12 mg/dL

 Avoid thiazide diuretics therapy, volume depletion,
prolonged bed rest or inactivity, and a high calcium diet
(>1000 mg/day).
Moderate hypercalcemia(12 and 14 mg/dL
 Follow as mild hypocalcemia
Severe hypercalcemia (calcium >14 mg/dL.
 Volume expansion with isotonic saline at an initial rate of
200 to 300 mL/hour that is then adjusted to maintain the
urine output at 100 to 150 mL/hou
Calcitonin 4IU/kg
The bisphosphonates(zoledronic acid
Hemodialysis –if ca >18-20mg/dl,neurologic sxs ,RF
 Treatments of hypocalcemia

• Asymptomatic hypocalcemia can be treated with oral or

IV calcium.

• Acute symptomatic hypocalcaemia should be treated

with IV 10% calcium gluconate

• NB. Associated deficits in magnesium, potassium, and pH

must also be corrected.

 Hypocalcaemia will be refractory to treatment if coexisting

hypomagnesaemia is not corrected first.

3.Phosphorus
• Normal 2.5-4.5 mg/dL
• Primary intracellular mineral
• Serum phosphate levels are tightly controlled by renal
excretion
• Influenced by parathyroid hormone and has inverse
relationship to Calcium
• abundant in metabolically active cells
• Regulation of Ca
• maintenance of acid-base balance
Hypophosphatemia-
 Causes  C/F:

– decrease in phosphorus • Impaired cardiac

intake (Malnutrition, function
malabsorption) • Poor tissue
– Hyperparathyroidism oxygenation
– Certain renal tubular defects • Muscle fatigue and
– Metabolic acidosis (esp. weakness
DKA) • N/V, anorexia
– Disorders causing • Disorientation, seizures, coma
hypercalcemia
 Treatment

 In asymptomatic patients with a serum phosphate less

than 2.0 mg/dL -give oral phosphate therapy
The treatment of symptomatic patients varies with the
severity of the hypophosphatemia:
 if the serum phosphate is 1.0 to 1.9 mg/dL –oral Rx
 if the serum phosphate is less than 1.0 mg/dL-IV Po4
Hyperphosphatemia  C/F :

 Causes
• Muscle cramping and
– Chronic renal failure (most weakness
common) • ↑ HR
– Hyperthyroidism,
• Diarrhea, abdominal
hypoparathyroidism
cramping, and nausea
– Severe catabolic states-
malignant hyperthermia
– Conditions causing
hypocalcemia
 Treatment

• Phosphate binders such as sucralfate or aluminum-

containing antacids can be used to lower serum phosphorus

levels.
• Calcium acetate tablets also are useful when
hypocalcemia is simultaneously present.
• Dialysis usually is reserved for patients with renal failure.
4. Magnesium
Normal 1.5 to 2.5 mEq/L
o Function:
 Important in CHO and protein metabolism
 Plays significant role in nerve cell
conduction
 Important in transmitting CNS messages and maintaining
neuromuscular activity
Hypomagnesaemia
Serum Mg<1.5meq/L
Causes
– ↓intake
– ↓ absorption; Acute pancreatitis,, malabsorption
syndrome, chronic alcoholism,total parenteral nutrition
– excessive loss through urinary, bowel elimination, burns,
primary aldosteronism,adminstration of amphotericin B
– Hypoparathyroidism with hypocalcemia
 Clinical manifestations

 hyperactive reflexes, muscle tremors, tetany, and positive

Chvostek’s and Trousseau’s sign)
 if Severe deficiency lead to delirium and seizures.
 ECG changes(prolonged QT and PR intervals, ST-segment
depression, flattening or inversion of P waves, torsades de
pointes, and arrhythmias)
NB. When hypokalemia or hypocalcemia coexists with
hypomagnesemia, magnesium should be aggressively replaced to
assist in restoring potassium or calcium homeostasis.
 Treatment

• oral if asymptomatic and mild.

• IV repletion is indicated if severe.
• For severe deficits (<1.0 mEq/L) or symptomatic,1
to 2 g of magnesium sulfate IV over 15 minutes.
NB. Simultaneous administration of calcium gluconate
will counteract the side effect of a rapidly rising
magnesium level and correct hypocalcaemia, which is
frequently associated with hypomagnesaemia
Hypermagnesemia
Serum Mg ++ level >2.5 mEq/L
Causes
 Excess intake with total parenteral nutrition (TPN),
 thermal injury, and
 severe acidosis(DKA),
 rarely massive trauma,

C/F
 N/V; hyporeflexia;
 neuromuscular dysfunction with weakness, lethargy,
 impaired cardiac conduction -hypotension & arrest.
 ECG changes(increased PR interval, widened QRS complex, and
elevated T waves)
 Treatments

• Eliminate exogenous sources of magnesium,

• correct concurrent volume deficits, and correct acidosis if

present.

• To manage acute symptoms, calcium chloride (5 to 10 mL) should

be administered to immediately antagonize the cardiovascular

effects.

• If elevated levels or symptoms persist,

hemodialysis may be necessary.

 fluid therapy

 To maintain adequate oxygen delivery to the tissue

 To maintain normal electrolyte concentration

 The type of fluid administered depends on

 The patient’s volume status

 Any concurrent electrolyte disorders

 Rate of fluid replacement

 Depends on the degree of dehydration.

 It should be fast until -the vital signs are corrected and

-adequate UOP is achieved

 Preoperative Fluid Therapy

 Appropriate preoperative fluid therapy improves optimal outcomes after

surgery,
 Maintenance therapy-
 Replacement therapy
 Daily requirement: Fluid maintenance
 For the first 0–10 kg- 100 mL/kg per day
 For the next 10–20 kg- 50 mL/kg /day
 For weight >20 kg-20 mL/kg / day
 Intraoperative Fluid Therapy

 Intra-operativelly fluid requirements depends on:

 Preoperative volume status & comorbidities
 Anesthetic technique
 Nature of the surgery
No accurate formula can predict intra-operative loss
Replacement of fluid during surgery often require 500-1000ml/hr of
balanced electrolyte solutions (Ringer's lactate)
The addition of albumin or other colloid containing solutions to
intraoperative fluid therapy is not necessary.
Blood loss- replaced by 3 ml of IV solution for every 1 ml of blood loss.
Redistribution and Evaporative surgical fluid losses
Intravenous Fluids

 IV fluids come in four different forms:

 Colloids
 Crystalloids

 Blood and blood products

 Oxygen-carrying solutions(on experiment

  Maintenance therapy
 Replacement therapy
 Special case therapy o Preferd regimen is:-
Maintenance Therapy:
 2L of 5%D/W
o Daily requirment by a 70kg man
 2.5-3 liters of water  1 L of N/S
 100-140 mmol of Na+&  20-30mmolof K+ added
 70 mmol of K+ are required
to each bag
In the preoperative fluid therapy; a frequently used
formula for calculating the volume of maintenance
fluids in the absence of pre-existing abnormality:-
Replacement Therapy:
 Is added to any maintenance regimen

1. Replacement of deficit

2. Replacement of continuing loss (estimated by the previous

24hrs loss)

Patients with acute blood loss require transfusion with packed

cells or whole blood.N.B colloids or saline may be used while
blood is being cross matched.
Special case therapy
 Heart failure: Risk of pulmonary edema if too much fluid is
given.

 Liver failure: despite being edematous and often hyponatremic,

have ↑ed total body sodium, and saline shouldn’t be used for
resuscitation, rather salt-poor albumin solution is preferred.
 1.Parenteral Solutions

The most common commercially available electrolyte

Hypertonic saline (7.5%):
 In patients with closed head injuries
 Increase cerebral perfusion and decrease intracranial pressure,
thus decreasing brain edema.
crystalloids
Considered in patients with
 hemorrhagic and septic shock,
 burn
 head injury
In undergoing plasmapheresis and hepatic resection Eg. RL, DNS,
D5W, NS
 Colloids

Are high-molecular-weight substances.

Tends to maintain these solutions intravascular(3-

6hrs) than crystalloid (30 min).

Indications for coloids
 severe intravascular fluid deficits (e.g. hemorrhagic shock) prior to the
arrival of blood for transfusion,
 severe hypoalbuminemia or conditions associated with large protein
losses such as burns.
 In burn pts, if the injury involves >30% of TBSA or if >3–4 L of
crystalloid has been given over 18–24 h post injury.

Eg.
 albumin, dextrans,
hetastarch, and Gelatins