Electrolytes such as sodium, potassium, calcium, and magnesium are important solutes in the body that regulate fluid balance and cell function. Sodium regulates fluid balance and is critical for nerve and muscle function. Hypokalemia can cause muscle weakness while hyperkalemia can cause cardiac arrhythmias. Calcium is needed for muscle and nerve function and its levels are tightly regulated. Magnesium plays a role in many biochemical reactions and body processes. Electrolyte imbalances can cause various clinical manifestations, so it is important to monitor, prevent, and treat electrolyte disorders.

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