Electrolyte Balance- Na. K. Ca. Mg. PO4 and post operative fluid management

1. ELECTROLYTES
DR NISHMA BAJRACHARYA
FCPS 1ST YR RESIDENT, OB/GYN

2. Copyright 2009, John Wiley & Sons, Inc.
Body Fluid Compartments

3. Electrolytes
• solutes that are found in various concentrations and measured in
terms of milliequivalent (mEq) units
• Can be negatively charged (anions) or positively charged (cations)

4. Sodium Na+
• 135-145mEq/L
• Major Cation, Chief electrolyte of the ECF
Determines ECF & ICF Osmolality
Serum osmolality = 2x Na+ + glucose/18 + urea/2.8
Normal – 275-290mOsm/kg
• Regulates volume of body fluids
• Needed for nerve impulse & muscle fiber transmission (Na/K pump)
• Regulated by kidneys/ hormones

5. HYPONATREMIA (Na+< 135mEq/L+)
ETIOLOGY
Hypervolemic Euvolemic
•CHF
•Cirrhosis
•Renal Failure
• Excessive administration of
hypotonic fluids
•Psychogenic polydipsia
•SIADH
•Drugs
•Withdrawal of gluococorticoids
•Pseudo hyponatremia

6. Hypovolemic
Renal Na conservation
(urine Na+ <20mEq/L )
Extra renal loss
•GI losses- vomiting,
diarrhea
•Skin losses- sweating,
burn
Renal Na wasting
(urine Na+ >20mEq/L)
•CRD
•Excessive diuretics
•Salt losing
nephropathy
•Adrenal insufficiency

7. • Mild 135-130 mEq/L
• Anorexia, Headache, Nausea, Vomiting, lethargy
• Moderate 130-125 mEq/L
• Personality Changes, Muscle Cramp Muscular weakness Confusion,
Ataxia
• Severe <125mEq/L
• Drowsiness, Diminished reflexes, Convulsions,Coma, Death

8. TREATMENT
HYPONATREMIA (correct underlying etiology)
HYPOVOLEMIA HYPERVOLEMIA EUVOLEMIA
Salt and water No salt Water restriction
supplementation Water restriction
Loop diuretics

9. ACUTE hyponatremia with severe neurological symptoms
• Rapid correction with hypertonic saline
1 – 2mEq/L /hr until Na reaches 125 mEq/L
Safe plasma Na+ concentration : 120-125mEq/L
• Correction using 3% NaCL (513 mEq/L)
• Na Requirement- 0.6 x total body weight x (desired Na – actual
Na)
TREATMENT

10. TREATMENT
Chronic asymptomatic hyponatremia (>48hrs):
• Rate of correction - 0.5 to 1.0 mEq/L/hour.
• MAX 8mEq/L per day.
• Rapid correction  Central pontine demyelination
Dysarthria, dysphagia, flaccid paralysis or coma
Diagnosed by CT or MRI (more accurate)

11. • Example- 71 Kg woman with neurologic symptoms has
serum Na 113 mEq/L,
• correction to serum Na level of 125 is achieved as follows
• 0.6 x 71 (weight) x (125- 113) = 511 mEq Na
• Patient requires 1 L of 3% saline to increase the level by
12 mEq
• Correction In 6-12 hrs appropriate
•

12. HYPERNATREMIA
(Na+>145mEq/L)
Etiology – Usually : water deficit
Hypernatremia associated with formation of concentrated
urine (U osm/ Posm >1.5 urine spc >1.015)
• Excess nonrenal water loss- Hot environment, fever,
hyperventilation- Urine output <35 ml/h
• Solute diuresis- due to inadequate water intake owing to
large volumes of renal solute excretion- Urine output >35
ml/h

13. • Hypernatremia associated with formation of dilute urine
(Uosm/Posm <1, sp gr <1.010)
• Renal loss
• Diabetes insipidus
• central (ADH deficiency) urine (Uosm/Posm <0.5, sp gr <1.005)
• Nephrogenic –
• Renal tubular Damage- ability to concentrate or dilute the urine is
decreased
when water loss exceed water intake- hypernatremia

14. CLINICAL FEATURES
Polyuria and thirst
Neurological symptoms: altered mental status, weakness,
neuromuscular irritability, focal neurological deficit,
seizures & coma
 Hypertonicity  contracts ICF volume  brain cell volume  subarachnoid
or intra-cerebral hemorrhage

15. TREATMENT
• Restoration of ECF volume using hypotonic solutions
• Water deficit :
Plasma Na+ concentration – 140
140
• Rate of correction : 0.5mEq/L/hr and not more than
10-12 mEq/l over 24 hours
X total body
water

16. POTASSIUM (K+)
3.5- 5.5 mEq/L
Determines excitability of nerves and muscle cells
including the myocardium.
Most abundant intracellular cation: 98% intracellular.

17. Poor intake Non renal loss Renal loss Redistribution
•Anorexia
•Starvation
•alcoholism
•Vomiting
•diarrhea
•nasogastric
aspiration
•Diuretics
•osmotic diuresis
• salt wasting nephropathy
• Mineralocorticoid excess
(primary or secondary),
Cushing’s syndrome,
• Steroid therapy
•Drugs- Gentamicin or
Amphotericin B
Metabolic alkalosis,
insulin, β2 agonist,
Hypokalemic
periodic paralysis,
Hypokalemia (K+ < 3.5mEq/L)

18. Clinical Features
• Commonly : Fatigue, myalgia and muscular weakness of
lower extremity
• Smooth Muscle : Constipation, ileus or urinary retention
• Progressive weakness, hyporeflexia, hypoventilation( due
to respiratory muscle involvement)

19. Early changes
Flattening or inversion of T waves
Prominent U waves
ST segment depression
Prolonged QT interval
Flattening of T waves

20. SEVERE HYPOKALEMIA
• Prolonged PR interval
• Decreased voltage
• Widening of QRS
• Ventricular arrythmia :VPC, ventricular tachycardia

21. TREATMENT
3.5 to 4 mEq/L :
• No potassium supplementation
• Add potassium sparing diuretics or decrease dose of diuretics
3 to 3.5 mEq/L :
• Treat in high risk groups
<3 mEq/L :
• Needs definitive treatment

22. IV KCl Therapy
 Reserved for symptomatic and severe cases
Common Guidelines
• Don’t give > 10- 20 mEq/L/ hour (typically 0.5mEq/kg/hr)
• Don’t give more than 240mEq/ day
• Continuous ECG monitoring required if using higher rate
• Use oral replacement whenever possible

23. TREATMENT
• KCL infusion : In NaCl not in 5% Dextrose
D5  insulin release  K+ shift ICS  aggravates hypokalemia(0.2-1.4mEq/L)
• K deficit-
• Kdeficit (mmol) = (Knormal lower limit - Kmeasured) x kg body weight x 0.4
• Daily K need- 1mmol /kg body weight
Example- A 70 Kg female with K+ 2.5 mEq/L requires correction as follows:
K deficit= (3.5- 2.5) x 70 x 0.4 = 28 mmol
Daily need- 1 x 70= 70 mmol
Total K to replenish over 24 hrs- 98 mmol

24. HYPERKALEMIA (K+ > 5.5mEq/L)
 Etiology
•Increased intake
o I.V fluids containing potassium- RL (4.0 mEq/L), Isolyte M
(35mEq/L)
o Transfusion of blood stored for prolonged periods
o High potassium containing foods
o Potassium containing Drugs- spironolactone

25. HYPERKALEMIA
• Tissue breakdown
Hemolysis, Rhabdomyolysis
Catabolic State
• Shift of potassium
Tissue damage
Metabolic acidosis
Uncontrolled Diabetes due to insulin deficiency
Hyperkalemic periodic paralysis, Succinylcholine

26. • Impaired Excretion
Acute renal failure or chronic renal failure
Drugs : Potassium sparing diuretic, ACE inhibitors, AT-II inhibitors,
Reduced tubular excretion : Addison’s disease, hyporeninemic
hypoaldosteronism and amyloidosis
• Pseuhohyperkalemia
Traumatic haemolysis during blood drawing
HYPERKALEMIA

27. CLINICAL FEATURES
 Muscle weakness  hyporeflexia  paralysis
affecting legs, trunk and arms (in that order) and
at last respiratory muscles.

28. Cardiac Arrythmia
6-7 mEq/L : Tall peaked T waves
7-8 mEq/L : loss of P waves, widening of QRS complex
8-10 mEq/L: QRS merges with T waves forming sine wave
 >9mEq/L : AV dissociation,
Ventricular tachycardia or
fibrillation , Diastolic arrest.

29. Severe elevation (7 mEq/L with toxic ECG changes)
• Calcium Gluconate 10% 10-20ml over 5-10mins
to reduce the effects of potassium at the myocardial cell
membrane (lowers risk of ventricular fibrillation)
Onset of action- few min
Avoid if patient is on digitalis.
TREATMENT

30. • Infuse 50gm glucose, 10 unit reg insulin and 50mEq
Sodium bicarbonate
• Onset- 15 min
• IV infusion- 500ml of 10 % dextrose + 15 units regular
insulin + 50 mEq NaHCO3- over several hours
• Nebulized albuterol: 10 to 20 mg nebulized over 15
minutes
Preferred in CRD for rapid lowering

31. • Na Polystyrene sulfonate (Kayexalate) by mouth, NG tube
(20-40 gm every 2-4 hrs)
• - ion exchange resin, that removes K by binding K and
releasing Na into body fluids
• Hemodialysis

32. …TREATMENT
For moderate elevation (6 to 7 mEq/L
- Reduce K intake, diuretics
- Kayexalate may be needed
- Correct metabolic acidosis/ hyperglycemia if present
- Stop administration of medications that can cause
increased K

33. CALCIUM
8-12 mg/dl
99% present in bones, 1% in cells and 0.15% in ECF.
40% bound to Plasma proteins
Unbound form or ionized- physiologic activity
Total calcium- measure of both bound and unbound
form

34. Mediates :Muscle contraction and nerve conduction
Functions in coagulation cascade
• PTH major hormone effecting Ca homeostasis (with
presence of Vit D)

35. HYPOCALCEMIA Ca <8-8.5mg/dl)
• Weakness
• Circumoral and distal paraesthesia
• Muscle spasm : carpopedal spasm, tetany.
• Mental changes: irritability, depression and psychosis.
• ECG- prolonged QT interval- can lead to heartblock or VF

36. CHOVSTEK’S SIGN

37. TROUSSEAU’S SIGN

38. ECG CHANGES

39. Causes
• Deficiency or absence of PTH
• Vit D deficiency
• Septic shock (suppression of PTH products)
• Renal failure
• Hyperphosphatemia

40. TREATMENT
Treat the underlying cause
Correct abnormalities in magnesium, potassium, and pH
simultaneously.
10% calcium gluconate 10 ml IV over 15 minutes.
+ IV infusion of 10-20 mL of 10% calcium gluconate) in 1000 mL
D5W @ 0.5 to 2 mg/kg/ hour (10 to 15 mg/kg).
Oral supplements- to treat long term

41. HYPERCALCEMIA
Serum calcium - 12 to 15 mg/dL.
Neurologic symptoms :
• Depression, weakness, fatigue, and confusion at lower levels.
• At higher levels : Hallucinations, disorientation, hypotonicity,
seizures, and coma.
Renal
• Polyuria , nocturia, stone formation

42. CLINICAL FEATURES
 Gastrointestinal symptoms:
• Dysphagia, Constipation, peptic ulcers, and pancreatitis
 Cardiovascular symptoms:
• Upto 15mg/dl myocardial contractility increases
• The QT interval typically shortens when the serum calcium is> 13mg/dL.
• PR and QRS intervals are prolonged.
• AV block may develop and progress to complete heartblock and even
cardiac arrest when the total serum calcium is > 15 to 20 mg/dL.
• Hypercalcemia can worsen digitalis toxicity and may cause hypertension.

43. Causes
• Hyperparathyroidism
• Thiazide diuretics, Vit D intoxication
• Malignancy
• - increased bone resorption and decreased renal excretion
• -metastasis to bones- increase in osteoclastic activity

44. TREATMENT
• Treat if
• Symptomatic and > 12mg/dl or >15mg/dl
• Immediate therapy
• Restore intravascular volume & promote excretion
• infusion of 0.9% saline at 250 to 500mL/h (saline diuresis) until any fluid
deficit is replaced and diuresis occurs (urine output 200 to 300 mL/h).
• After adequate rehydration, 3-6 L/day.
• Addition of loop diuretics – increase urine calcium excretion

45. TREATMENT
Biphosphonates – inhibit osteoclast precursors
Eg- Etidronate Disodium, pamidronate, zoledronic acid
Calcitonin- inhibit renal excretion of calcium and inhibits
osteoclastic activity
Glucocorticoids- decrease intestinal absorption of Ca, promote
urinary excretion

46. MAGNESIUM
Magnesium is the fourth most common mineral
second most abundant intracellular cation
Normal serum Mg2+ 1.2 – 2.2mg/dl
Magnesium is necessary for the
• movement of sodium, potassium, and calcium into and out of cells
• magnesium plays an important role in stabilizing excitable membranes.
• Enzyme co-factor in protein and carbohydrate metabolism
Reabsorbed in ascending limb of Loop of Henle, less in PCT and DT

47. Obstetric practice
• Powerful tocolytic – Manage premature labour.
• Prophylaxis and treatment of eclampsia.

48. HYPOMAGNESEMIA <1.8mg/dl
Result from decreased GI absorption due to chronic diarrhea,
malabsorption , NG suction
Muscular tremors and fasciculations, Tetany
Altered mental state
Cardiac arrhythmias such as torsades de pointes.
Often seen together with hypocalcemia, hypokalemia
ECG findings- prolonged PT and QT intervals

49. TREATMENT
For severe or symptomatic hypomagnesemia:
1 to 2 g of IV MgSO4 over 5 to 20 minutes.
• Followed by continuous infusion of 1mEq/kg/24hours.
For seizures (Eclampsia) – loading dose 4 g IV MgSO4 (20%) over 5
mins followed by 10 gm MgSO4( 50%) deep IM
Maintenance- 5gm MgSO4 (50%) IM 4 hrly
Administration of calcium is usually appropriate because most
patients with hypomagnesemia are also hypocalcemic.

50.  Caution and monitoring MgSO4 therapy
• Check deep tendon reflex every 15mins (knee jerk)
• Periodic monitoring of serum Mg concentration.
• Reduce dose in renal failure.
• Contraindicated in heart block or extreme myocardial damage
• Maintain urine output – >30ml/hr
• Overtreatment  10% calcium gluconate 10-20ml followed by
fluid loading and diuretics.
TREATMENT

51. HYPERMAGNESEMIA (>3mg/dl)
 Etiology
• Renal failure patients : most common cause
• Treatment of pre-eclampsia with I.V MgSO4.
• Therapy with Mg containing antacids,
laxatives.

52. CLINICAL FEATURES
• Nausea vomiting, somnolence
• Muscular weakness muscular paresis leading to respiratory
depression and respiratory failure.
• Hypotension: peripheral vasodilatation
• Bradyarrhythmia, asystole
• ECG changes- Prolonged PR interval, QRS duration and QT
interval, Complete heart block

53. TREATMENT
Eliminate source
10% calcium gluconate 10-20 ml IV over 10 min
IV saline diuresis (administration of IV normal saline and furosemide
[1 mg/kg]) can be used to increase renal excretion of magnesium until
dialysis can be performed.
Dialysis is the treatment of choice for severe hypermagnesemia.
Artificial respiration

54. PHOSPHORUS
3-4.5 mg/dl
Major Buffer anion for ICF & ECF
• Rapid shifting can occur
Functions
• Muscle, red blood cells & nervous system
• Maintains acid-base balance
Adequate renal function necessary to maintain normal balance by PTH
 90% excreted by kidneys

55. HYPOPHOSPHATEMIA<2.5mg/dl
• Paresthesia, Muscle pain/weakness
• Confusion/coma
• Causes- malabsorption, Vit D deficiency,
Hyperparathyrodism

56. TREATMENT
Diet/supplements (mild)
IV replacement (severe)- infusion 2.5 – 5 mg
elemental phosp/ kg every 6 hrs
• Concomitant Ca supplements

57. HYPERPHOSPHATEMIA (> 4.5mg/dl)
• Tachycardia, Restlessness
• Anorexia, Nausea and vomiting
• Tetany, Tingling & numbness of fingers/lips
• Muscle spasms
• Causes- renal failure, rhabdomyolysis, tumor lysis
syndrome, hypoparathyroidism

58. TREATMENT
Diet restrictions
Administer phosphate binding products
• Calcium acetate and calcium carbonate or aluminum
hydroxide
Dialysis in severe renal failure.

59. FLUID AND ELECTROLYTES IN POST OPERATIVE
PERIOD

60. • After surgery modification in normal physiology of fluid
and electrolytes balance.
• ACUTE STRESS increased sympathetic stimuli-
tachycardia, vasoconstriction & stress.
• Increased ACTH stimulate adrenal gland
• --secretes large amount of hydrocortisone to fight acute
stress and aldosterone which leads to Na retention and
urinary loss of K.

61. • Increased ADH secretion causes water retention ,
reduction in U.O to as low as 500 ml on 1st post op day.
• NPO status leads to hypovolemia prior to surgery, pt
becomes hypotensive during surgery & anaesthesia.
• Fluid loss
• Surgical stress or direct damage of kidney, brain ,lung ,
skin or GI tract.

62. 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.

63. When and how long to give post-op iv fluid ?
• Short operative procedure ( no handling of intestine or viscera )
– maintenance i.v fluid to correct deficit due to NPO 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 OBS/GYNE surgeries – I.V fluid is required for only 24 to 48
hrs.

64. Factors to consider for 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 ( HT,DM) and associated
electrolytes and acid base disorders, if any.
• Insensible loss due to atmospheric temp, pyrexia,
hyperventilation etc.

65. On the 1st post op day
Increased ADH and aldosterone secretion –salt and fluid
retention by the kidney .
K is avoided in I.V fluids
So preferred- 5% dextrose, isotonic saline
• Maintenance fluid - steady rate over an 18 to 24 hrs
period.

67. Volume Excess
• Blood excess – pulmonary congestion.
• Saline excess- weight gain, periorbital puffiness,
hoarseness or dysnoea on exertion.
• Hypotonic fluid excess ( 5% dextrose) – hyponatremia

68. Fluid volume deficit
• Decreased U.O < 30 ml/hr
• Postural hypotension
• Tachycardia
• Diminished skin turgor
• Decreased capillary refill time
• Inc BUN out of proportion to creatinine
TREATMENT
Depends on the type of fluid lost , can be done with isotonic solutions –NS or LR.

69. Electrolyte Imbalances
• Hyponatremia-
• Excess ADH- retention of water In excess of sodium.
• Excess 5% dextrose
• Water administration consistently which exceeds water loss.
• Nausea without vomiting, drowsy, weak, confused or gets convulsion.
TREATMENT
Avoid using hypotonic solution.
Avoid excessive use of electrolyte free solutions during the first 2-4 post
op days.

70. • Hypokalemia – most common
• Lost through urine or GI.
• Post op infusion of mannitol or diuretics.
• Prolonged administration of potassium free i.v fluids.
• Extreme weakness , muscular hypotonia , paralytic ileus.
Treatment
Daily supplement 60 -100 mEq QD.
• Hypernatremia and Hyperkalemia – Uncommon

71. Fluid management in Hypertension
• Strictly over 24 hrs and not faster.
• Sodium containing fluids cause water retention and rise in B.P
• Strict B.P monitoring should be done on 1st post op day.
• Furesemide will drop the b.p , increase the urine output but can
cause disturbance in electrolyte levels.

72. Fluid management in Diabetes
• high chances of development of diabetic ketoacidosis.
• Avoid using dextrose on 1st post op day as already due to
excess glucocorticoids the level of glucose is on the
higher side.
• GKI drip.

73. References
• Te linde’s Operative Gynecology, 11th Edition
• UpToDate.com

74. Thank you