To help understand the need for Iv fluid therapy and electrolyte imbalances and their correction in surgical patients. It aims to keep the patient well hydrated with good urine output and avoid vital sign derangements and to avoid complications of wrongly advised fluids.

2. FLUID AND ELECTROLYTE
BALANCE
DR ADNAN BILAL
PGR SU-III

3. GOAL OF FLUID THERAPY
• AIM TO MAINTAIN
• B.P >100/70 mm of hg
• Pulse rate of less than 120 bpm
• Hourly U.O between 30 and 50 ml
• Normal temperature, warm skin , normal respiration and sensorium

4. WHEN AND HOW LONG TO GIVE POST-OP IV FLUID
THERAPY?
• Short operative procedure ( no handling of intestine or viscera ) – maintenance IV fluid to
correct deficit due to NBM state. After 4-5 hours oral fluid is restarted & iv fluid is not needed.
• Major surgeries ( handling of intestinal viscera ) – requires post op iv fluid for few days. After
ensuring normal movement of intestine oral fluid intake is restarted.
• Major surgery ( handling of intestinal viscera not done ) most of OBG surgeries – IV fluid is
required for only 24 to 48 hrs.

5. WHICH FACTORS TO BE CONSIDERED BEFORE
WRITING POST OP IV FLUID?
• Age , weight , vital data, hydration status and U.O.
• Nature of surgery, blood loss , nature and vol of fluid and blood replaced intraoperatively.
• Drain output , fluid lost at operative site.
• Renal status, associated illness ( HTN, DM) and associated electrolytes and acid base disorders, if
any.
• Insensible loss due to atmospheric temp., pyrexia and hyperventilation etc.

6. • WATER CONSISTS OF 60% OF TOTAL BODY WEIGHT, IN HEALTHY YOUNG MALE ADULT
• Relationship of total body weight and total body water is a reflection of body fat.
• Lean tissue have higher water content
• Muscle
• Solid organs
• Low water content in bone and fat
• Young, lean, male => high water content
• Deuterium => used for to measure TBW by dilution
• Female TBW is ~ 50% because of ↑ adipose tissue and ↓muscle mass
• TBW is additionally corrected by
• ↓ 10-20% in obese
• ↑ 10% in malnutrition
• The highest TBW is in the new born=> 80%, decreases to 65% at 1 year and remains constant.

7. FLUID COMPARTMENT
Total Body water
(60 % 0f TBW)
Intracellular = 2/3
(40% of TBW)
Extra-cellular = 1/3
(20% of TBW)
Interstitial = ¾
(15% of TBW)
Plasma = ¼
(5% of TBW)

9. COMPOSITION OF FLUID
COMPARTMENTS
ECF:
• Na+ (Principle cation)
• Cl & HCO3 (Principle anions)
ICF:
• K & Mg (Principle cations)
• PO4 & SO4 (Principle anions)
• Negatively Charged Proteins

10. CONTINUED…
• Concentration gradient is maintained by Na/K ATPase pump
• Diffusion of ions and protein is restricted but water diffuses freely, thus volume
increment in water increases the volume of all compartments
• Na is confined to the ECF and is strongly associated with water, thus administration
of a Na containing fluid increases the volume of plasma and interstitial fluid
(expanded 3X↑)

11. OSMOLALITY & TONICITY
• Osmolality
• Number of osmoles of solute particles per kilogram of water
• Effective
• Ineffective
Effective osmoles cannot freely permeate cell membranes and are therefore restricted to either the
intracellular or extracellular fluid compartments. The asymmetry in effective osmoles between these
compartments causes the movement of water across the cell membrane.
• Tonicity:
• Effective osmolality of a solution is equivalent to its tonicity.
• It is the parameter the body attempts to regulate.

12. PARENTERAL FLUID THERAPY
• Normal individual
• Consumption: Average of 2,000 to 2,500 ml of water daily
• Losses: Approximately 1,000 to 1,500 ml in urine and 250 ml in stool
• Minimum amount of urinary output required: 800 ml
• Insensible water loss (skin and respiratory tract): 750 ml +
• Hypermetabolism
• Fever
• Hyperventilation

13. FLUID MAINTENANCE
Target: To maintain a urine output of 0.5 to 1 ml/kg/hour in adults
On the basis of body weight as follows:
• 100 ml/kg/day for the first 10 kg
• 50 ml/kg/day for the second 10 kg
• 20 ml/kg/day for each subsequent 10 kg
Maintenance fluids in general should contain:
• Na+ (1 to 2 mmol/kg/day)
• K+ (0.5 to 1 mmol/kg/day)

14. INTRAOPERATIVE FLUID MANAGEMENT
Requires replacement of:
1. Preoperative deficit
2. Ongoing losses in intraoperative phase
• Maintenance fluids for the length of the case
• Hemorrhage
• Third-space losses
✓ Acute blood loss can be replaced with a volume of crystalloid that is 3 to 4 times the blood loss or with an equal
volume of colloid or blood.
✓ Intraoperative insensible and third-space fluid losses depend on the size of the incision and the extent of tissue
trauma.
• Small incisions with minor tissue trauma (e.g., Inguinal hernia repair): ~1 to 3 ml/kg/hour
• Medium-sized incisions with moderate tissue trauma (e.g., Uncomplicated sigmoidectomy) : ~ 3 to 7 ml/kg/hour
• Larger incisions and operations with extensive tissue trauma and dissection (e.g., Pancreaticoduodenectomy): ~ 9 to 11
ml/kg/hour or greater

15. POSTOPERATIVE FLUID MANAGEMENT
• Kidneys retain Na+ ions after surgery or any stressful condition due to release of adrenocortical
hormones and high levels of ADH in early post-op period leading to K+ conservation. So in early post-
op period 5% D/W should be advised and K+ should be added after 24 hours if urine output is
adequate.
• Titrated to maintain an adequate urine output (0.5 to 1.0 ml/kg/hour)
• GI losses that exceed 250 ml/day from nasogastric tube suction should be replaced with an equal
volume of crystalloid.
• Mobilization of perioperative third-space fluid losses typically begins 2 to 3 days after operation.
• In general, gastric losses:
• Replaced with D5 1/2 NS with 20 mEq K
Pancreatic, biliary, largest intestine losses (e.g., Diarrhea) and small intestine losses
• Replaced with lactated ringer (LR) solution

17. CRYSTALLOIDS
• Contain sodium as the major particle
▪ Isotonic crystalloids
• Distribute uniformly throughout the extracellular fluid compartment (25% in ECF after 1 hour)
• Both LR and NS can be used interchangeably
• Ringer Lactate (LR):
• Mimic extracellular fluid
• Provides a HCO3 – precursor so is useful for replacing GI losses and extracellular fluid volume deficits
• Normal saline (NS) Preferred:
• Hyperkalemia
• Hypercalcemia
• Hyponatremia
• Hypochloremia
• Metabolic Alkalosis

18. ▪ Hypertonic saline solutions
• Resuscitation fluids for patients with shock or burns
• Smaller quantities are required for resuscitation
• Possible side effects:
• Hypernatremia
• Hyperosmolality
• Hyperchloremia
• Hypokalemia
• Central Pontine Demyelination With Rapid Infusion
• Need cautious administration
▪ Hypotonic solutions (D5W & 0.45% NACL)
• Distribute throughout the TBW compartment, expanding the intravascular compartment by as little
as 10% of the volume infused.
• Used to replace free water deficits (as in hypernatremia)

19. COLLOIDS
• Contain high-molecular-weight substances that remain in the intravascular space
• More prompt restoration of tissue perfusion and may lessen the total volume of fluid required for
resuscitation
• More expensive than crystalloids
• Use of colloids is indicated when substantial amounts of crystalloids fail to sustain plasma volume
▪ Albumin preparations
• 25% albumin (100 ml) & 5% albumin (500 ml) expand the ICF volume by an equivalent amount (450
to 500 ml).
• Albumin 25% is indicated in the edematous patient to mobilize interstitial fluid into the intravascular
space.
• Not indicated
• Adequate colloid oncotic pressure (serum albumin >2.5 mg/dl, total protein >5 mg/dl)
• For augmenting serum albumin in chronic illness (cirrhosis or nephrotic syndrome)
• As a nutritional source

20. ▪ Dextran
• Synthetic glucose polymer
• Volume infused = Intravascular volume expansion
• Side effects
• Renal Failure
• Osmotic Diuresis
• Coagulopathy
• Laboratory Abnormalities (e.g. Elevations in blood glucose & protein and interference with blood cross-
matching)
▪ Hydroxyethyl starch (Hetastarch)
• Synthetic molecule resembling glycogen
• Increases the intravascular volume by an amount equal to or greater than the volume infused
• Increased incidence of acute kidney injury
• No benefit or detrimental effects of Hetastarch

22. ELECTROLYTE IMBALANCE & TREATMENT
➢ Sodium (NA+)
• Principle cation in ECF
• Normal serum Na+ concentration is 135 to 145 mmol/L (310 to 333 mg/dl)
• Sodium balance is maintained primarily by the kidneys
• Responsible for 90% of plasma oncotic pressure
▪ Hyponatremia
• Symptoms: neurologic e.g. lethargy, confusion, nausea, vomiting, seizures and coma.
• Can occur due to:
• ↑ in TBW
• ↓ Serum Na+ concentration

23. ▪ Isotonic hyponatremia
• Hyperlipidemic and hyperproteinemic states result in an isotonic expansion of the circulating
plasma volume and cause a decrease in serum na+ concentration, although total body Na+
remains unchanged.
• Corrects with resolution of the underlying disorder
▪ Hypertonic hyponatremia
• Rapid infusion of hypertonic solutions of glucose, mannitol, or glycine may result in a transient fluid
shift from the intracellular to the extracellular compartment, thereby diluting serum Na+
concentration
• Corrects with resolution of the underlying disorder.
▪ Hypotonic hyponatremia
• Hypovolemic hypotonic hyponatremia
• Hypervolemic hypotonic hyponatremia

24. ▪ Hypovolemic hypotonic hyponatremia
• Most commonly results from replacement of sodium-rich fluid losses (e.g., From the GI tract, skin or lungs) with
an insufficient volume of hypotonic fluid (e.g., D5W and 0.45% NaCl).
• Can be managed with administration of 0.9% NaCl to correct volume deficits and replacing ongoing losses.
• Hypervolemic hypotonic hyponatremia
• Edematous states of congestive heart failure, liver disease, and nephrosis occur in conjunction with inadequate
circulating blood volume serving as a stimulus for the renal retention of Na+ and Water. Disproportionate
accumulation of water results in hyponatremia.
• May respond to water restriction (1,000 ml/day) to return Na+ to greater than 130 mmol/L (299 mg/dl).
• Optimizing cardiac performance may assist in Na+ correction
• Plasma Na+ can be increased to a safe level by the use of a loop diuretic (furosemide, 20 to 200 mg
intravenously every 6 hours) while replacing urinary Na+ losses with 3% NaCl. If patient becomes
symptomatic.
• Synthetic brain natriuretic peptide (BNP) is also useful therapeutically in the setting of acute heart failure.

25. ▪ Isovolumic hypotonic hyponatremia
▪ Water Intoxication
• Excessive water intake (Psychogenic polydipsia)
• Mildly impaired renal function (primary polydipsia)
• Administration of large quantities of hypotonic fluid in the patient with renal failure
• Water intoxication responds to fluid restriction (1,000 ml/day)
▪ Hypokalemia
• GI fluid loss or secondary to diuretics
▪ Reset osmostat
• Normally, the serum osmostat is set at 285 mosm/L. In some individuals with chronic disease (e.g.,
Cirrhosis), the osmostat is reset downward, thus maintaining a lower serum osmolality.
• Respond normally to water loads with suppression of ADH secretion and excretion of free water.

26. ▪ SIADH
• Characterized by low plasma osmolality (100 mOsm/kg), elevated urine Na (>20 mEq/L), and
clinical euvolemia.
• Causes include
• Pulmonary disorders (e.g., Atelectasis and respiratory failure)
• Central nervous system disorders (e.g., Trauma and meningitis)
• Drugs (e.g., Cyclophosphamide and cisplatin)
• Ectopic ADH production (e.g., Small-cell lung carcinoma)
For SIADH, water restriction (1,000 ml/day) should be attempted initially. The addition of a loop
diuretic (furosemide) or an osmotic diuretic (mannitol) may be necessary.
▪ Transurethral resection syndrome
• Results from intraoperative absorption of significant amounts of irrigation fluid

27. EXTREME HYPONATREMIA
• In the presence of symptoms or extreme hyponatremia (Na+ <110mmol/L [253mg/dl]) hypertonic
saline (3% NaCl) is indicated.
• Serum Na+ should be corrected to approximately 120 mmol/L (276 mg/dl). The quantity of 3%
NaCl that is required to increase Serum Na+ to 120 mmol/L can be estimated by calculating the
Na+ deficit:
• Use of a loop diuretic (furosemide, 20 to 200 mg intravenously every 6 hours) may increase the
effectiveness of 3% NaCl administration.
• In patients with severe acute hyponatremia, the initial correction rate should not exceed 1 to 2
mmol/L/hour. In the first 48 hours, normo- or hypernatremia should be avoided

29. ▪ Hypernatremia
• Symptoms: Lethargy, weakness, and irritability and may progress to fasciculations, seizures, coma,
and irreversible neurologic damage
• Hypovolemic hypernatremia
• Causes
• Diuresis
• GI, Respiratory, And Cutaneous (Burns) fluid losses
• Chronic renal failure
• Partial urinary tract obstruction
• Adipsic
Replacement of free water is the main goal of treatment. Water deficit can be calculated by:

30. • Rapid correction can result in cerebral edema and permanent neurologic damage.
• Only one half of the water deficit should be corrected over the first 24 hours, with the remainder
being corrected over the following 2 to 3 days. If oral intake is not possible, D5W or D5 0.45%
NaCl can be substituted.
▪ Hypervolemic hypernatremia
Results from:
• Parenteral administration of hypertonic solutions (e.g., NaHCO3, saline, medications and nutrition)
• Aldosteronism
• Cushing disease (secondary hypercortisolism)
• Mineralocorticoid excess.
In cases of hypervolemic hypernatremia, free water replacement can be supplemented with a loop
diuretic.

31. ▪ Isovolumic hypernatremia
Hypotonic losses
• Evaporative losses from the skin and respiratory tract
• Urinary free water losses
• Require the administration of approximately 750 ml of electrolyte-free water (e.g., D5W) daily to parenterally
maintained afebrile patients
Diabetes insipidus
• Polyuria and polydipsia in association with hypotonic urine (urine osmolality 287 mOsm/kg)
• Central diabetes insipidus: Defect in the hypothalamic secretion of ADH
• Nephrogenic diabetes insipidus: Renal insensitivity to normally secreted ADH
• Treatment involves removal of any potentially offending drug and correction of electrolyte abnormalities. Dietary
sodium restriction in conjunction with a thiazide diuretic may be useful (hydrochlorothiazide, 50 to 100 mg/day
orally).
Therapeutic
• Deliberate hypernatremia by administration of hypertonic saline to control elevated intracranial pressure and
cerebral edema after head injury.

33. • Potassium
• Major intracellular cation
• The normal serum concentration is 3.3 to 4.9 mmol/L (12.9 to 19.1 mg/dl).
• Approximately 50 to 100 mmol (195 to 390 mg/dl) K+ is ingested and absorbed daily. Ninety
percent of K+ is renally excreted, with the remainder eliminated in stools.
• Hypokalemia
• Clinical Manifestation:
• Mild hypokalemia (K+ =/>3 mmol/L) generally asymptomatic.
• Symptoms occur with severe K+ deficiency (K+ < 3) and are primarily cardiovascular.
• Early ECG manifestations include ectopy, T-wave depression, and prominent U waves.
• Severe depletion increases susceptibility to reentry arrhythmias.
• Causes:
• GI losses, renal losses, and cutaneous losses (e.G., Burns)
• Insulin excess, metabolic alkalosis, myocardial infarction, delirium tremens, hypothermia, and theophylline
toxicity ( cause increase K+ uptake intracellularly)
• Refeeding syndrome

34. TREATMENT
• Mild hypokalemia, oral replacement is suitable.
• Daily therapy: 40 to 100 mmol (156 to 390 mg) oral potassium chloride in single or divided doses
(with intact renal function).
• In severe depletion, parenteral therapy is indicated by using K+ concentrations (administered as
chloride, acetate, or phosphate) in peripherally administered intravenous fluids should not exceed
40 mmol/L (156 mg/dl) = 2 ampoules, and the rate of administration should not exceed 20 mmol
(78 mg)/hour.
• Never Inject K+ as a bolus dose

35. ▪ Hyperkalemia
• Serum K+ levels of more than 5mmol/L.
• Causes:
• Insulin deficiency
• β-adrenergic receptor blockade , ACE inhibitors & Spironolactone use
• Rhabdomyolysis
• Cell lysis (after chemotherapy)
• Digitalis intoxication
• Reperfusion of ischemic limbs
• Succinylcholine administration
• Renal failure
• Burns
• Addison's disease
• Pseudo-hyperkalemia
• Hemolysis

36. Clinical manifestations:
• Mild: Generally asymptomatic
• Significant hyperkalemia: Symmetric peaking of T waves, reduced p-wave voltage, and widening
of the QRS complex. If untreated, severe hyperkalemia ultimately may cause a sinusoidal ECG
pattern.
Treatment:
• Mild hyperkalemia (K+= 5 to 6 mmol/L)
• Reduction in daily K+ intake
• Addition of a loop diuretic (e.g., Furosemide) if needed.
• Any medication that is capable of impairing K+ homeostasis should be discontinued, if possible.
• Severe hyperkalemia (K+ >6.5 mmol/L)
• Temporizing measures
• Therapeutic measures

37. ✓ Temporizing measures:
• Produce shifts of potassium from the extracellular to the intracellular space
• Calcium gluconate 10% (5 to 10 ml intravenously over 2 minutes) should be administered to patients with
profound ECG changes who are not receiving digitalis preparations.
• NaHCO3 (1 mmol/kg or 1 to 2 ampules [50 ml each] of 8.4% nahco3) can be infused intravenously over a 3-
to 5- minute period and can be repeated after 10 to 15 minutes if ECG abnormalities persist.
• Dextrose (0.5 g/kg body weight) infused with insulin (0.3 unit of regular insulin/g of dextrose) transiently
lowers serum K+ (the usual dose is 25 g dextrose, with 6 to 10 units of regular insulin given simultaneously as
an intravenous bolus).
• Inhaled β-agonists (e.g., Albuterol sulfate, 2 to 4 ml of 0.5% solution [10 to 20 mg] delivered via nebulizer)
have been shown to lower plasma K+, with a duration of action of up to 2 hours.
✓ Therapeutic measures
• Definitively decrease total body potassium by increasing potassium excretion
• Sodium polystyrene sulfonate (kayexalate) is a Na+/K+ exchange resin. A decrease in serum K+ level
typically occurs 2 to 4 hours after administration; however, use with caution as it has been associated with
bowel necrosis.
• Hydration with 0.9% NaCl in combination with a loop diuretic (e.g., Furosemide, 20 to 100 mg intravenously)
should be administered to patients with adequate renal function to promote renal K excretion.
• Dialysis is definitive therapy in severe, refractory, or life-threatening hyperkalemia.