1. Electrolyte Disturbances
In ICU
Dr. Fathia Hassan Khalil

2. Body Fluids
• The average body water is 60% of TBW
• 65% in males & 55% in females
• In obese patient it decrease 5%

3. Sodium

4. Sodium
• Sodium is the major ion in ECF
• Normal value in blood is 135 : 145 mMol/L

5. Sodium is responsible for:
• 1- Maintaining plasma & ECF osmolality
• 2- Maintaining i.v. & ECF volume
• 3- Has physiologic role in generation of
• Membrane resting potential
• Action potential
• Glucose & a. a. transport.

6. Sodium concentration is regulated by:
• Renal system
• Endocrine system

7. • Renal excretion of sodium is adjusted to
equal the amount ingested.
• Urine sodium output 1 - 400 mEq/day
• The normal is 90 mEq/d

8. • In the kidney 96-99 % of the filtered
sodium is reabsorbed
– 67% in PCT by active process
– 25% in thick ascending loop of Henel
passively (loop diuretics acted upon)
– 5% in DCT & 3% in CD in exchange with K &
Cl (controlled by aldosteron).

9. Hyponatremia

10. Hyponatremia
• Hyponatremia means serum sodium less
than 130 mEq/L
Less than 130 Mild
• Less than 125 Moderate
• Less than 115 Severe

11. • No linear correlation between degree of
hyponatremia and symptoms.
• Symptoms depend upon the rapidity of
occurrence of hyponatremia.

12. Because of difference between the
regulation of total body volume and
sodium concentration, it is possible to
have hypo- or hypernatremia in face of
hypo-, hyper-, or euvolemia.

13. Classification of Hyponatremia
I- Hyponatremia with normal serum
osmolality
II- Hyponatremia with high serum osmolality
III- Hyponatremia with low serum osmolality

14. I-Hyponatremia with normal serum
osmolality
• S. Osmolality: 280-295 mOsm/kg water
• Called Pseudohyponatremia
• Causes:
– 1- Hyperlipidemia (every 4-6 gm/L increase in
lipids leading to 1mEq/L decrease in sodium.
– 2- Hyperproteinemia e.g. multiple myeloma
(every 10gm/dl increase leading to 1mEq/L
decrease in serum sodium).

15. II-Hyponatremia with High Serum
Osmolality
S. Osmolality: > 295mosm/kg water
• Called Hypertonic Hyponatremia
Caused by increase impermeant solutes
replacing sodium in the blood

16. • Causes:
1-Non sodium solutes e.g.
glucose, mannitol, and some toxins
(ethanol & urea).
2- Renal failure due to impaired water
excretion.

17. Management of Hyponatremia with
normal & High S. Osmolality
- Restoration of volume and free water deficit
- Treatment of non-sodium salts e.g. toxins
- Treatment of hyperglycemia or mannitol level
- Treatment of hyperlipidemia or
hyperprotenemia.

18. III-Hyponatremia with
Hypoosmolality
• S. Osmolality : < 280 mosm/kg water
• It is the most common type
• It means that free water intake more than
water loss

19. Types of Hyponatremia with Hypo-
osmolality
• Based on clinical assessment of total body
water and sodium content it is classified
into:
1. Hypovolemic hypoosmolar hyponatremia
2. Hypervolemic hypoosmolar
hyponatremia
3. Euvolemic hypoosmolar hyponatremia

20. 1-Hypovolemic Hypoosmolar
Hyponatremia
• Causes:
• 1- Renal causes
• Diuretic use
• Renal tubular dysfunction
• Hypoaldosteronism
Urine sodium > 30mEq/L
Urine osmolality normal (300:400)

21. • 2- Non renal causes:
• G.I. loss
• Skin loss
• Dietery sodium restriction
• Third spacing
Urine sodium < 15mEq/L
Urine osmolality > 400 mosm/kg w

22. Manifestations of Hypovolemic
Hypoosmolar Hyponatremia
• Intra vascular volume depletion
• Hypotension
• Orthostatic hypotension
• Tachycardia
• Skin dehydration

23. Management of Hypovolemic
Hypoosmolar Hyponatremia
• - Replace the volume depletion to depress
ADH by isotonic crystalloid, or colloids and
blood if not enough.
• -Replace free water with sodium by Water
restriction and Furosemide
• Replace urine output by isotonic or
hypertonic saline

24. 2- Hypervolemic Hypoosmolar
Hyponatremia
• It is called dilutional hyponatremia
• Causes:
• CHF
• Liver cirrhosis
• Nephrotic syndrome

25. Manifestations of Hypervolemic
Hypoosmolar Hyponatremia
• Total body water increased and the patient
is edematous but
• The effective circulatory volume is low.
• Urine sodium < 15 mEq/L
• Urine osmolality > 400 mosm/kg w

26. Management of Hypervolemic
Hypoosmolar Hyponatremia
• The aim of management is to improve
• The effective circulating volume
• Renal function
• Cardiac function
• Distal tubular delivery of sodium
*Combination of furosemide & ACE
Inhibitor.

27. 3-Euvolemic Hypoosmolar
Hyponatremia
* Syndrome of inappropriate ADH secretion
• Excess ADH secretion
• Secretion stimulated by non-osmotic,
non-volumic factors e.g.:
– Emotional stress
– Endocrine disorders
– CNS diseases
– Excess hypotonic fluids
– Drugs e.g. NSAID & Carbamezapine
• Urine Na > 30mEq/L, U. Osm > 400mosm

28. Management of Syndrome of
inappropriate ADH secretion
• Treatment of the cause e.g. brain tumor
resection
• Free water restriction
• Furosemide to get –ve water balance
• Replace fluid by isotonic or hypertonic
saline
• Measure serum sodium every 6:12 h.

29. • * Water intoxication: e.g.
• Psychosis
• Heavy beer drinking
• Absorption of hypoosmolar fluids
during prostate resection.
• Urine osmolality < 100 mosm/kg w
• Treated by water restriction

30. General Manifestations of
Hyponatremia
• Serum osmolality and cellular dehydration
are the main insult done
• CNS cells are the most affected by
changes in osmolality.
• CNS compensate for slow changes in
osmolality affected severely in acute
changes.

31. General Manifestations of
Hyponatremia
• In acute hyponatremia:
• -CNS manifestations:
• begin by lethargy & confusion up to
seizures, cerebral edema & coma
• GI symptoms
• Muscle cramps & weakness

32. Management of Hyponatremia

33. Management Based on:
*Treatment of the cause
*Restoration of serum sodium
concentration
*Normalization of serum osmolality

34. Correction of Serum Sodium
Acute changes in sodium concentration
should be treated rapidly, but
• Chronic changes should be treated more
slowly.

35. In acute hyponatremia (<2 days):
Correct by no faster than 1 : 2 mMol/L/h
Serum sodium not increased more than 130
mEq/L and avoid hypernatremia
In presence of seizures or increase ICP the
correction could be in 3 :4 mMol/L in the
first hour or even 8 mMol/L

36. In chronic hyponatremia:
Correct by less than 12 mMol/L/day
The rapid correction may leads to:
Osmotic Demyelination Syndrome
Severe neurological deterioration after one
to several days of rapid correction.

37. • The amount of sodium required to increase
serum sodium concentration is calculated
as the equation:
• Na required=
(Desired Na – Present Na) * TB Water
• TB Water =
• BW * 0.6 in male (0.5 in female)

38. • The desired sodium should not exceed
130mEq/L
• Hypertonic saline used only in severe
hyponatremia
• Hypertonic saline should be stopped when:
• Pt become asyptomatic
• Plasma sodium increased by 20 mmol/L
• Plasma sodium reached to 120:125mmol/L

39. Hypernatremia

40. Hypernatremia
• It means s. sodium >150 mEq/L
• It results from loss of free water or
• Gain of sodium ions in excess of water

41. Risky patients are:
• The extreme of age for inability to drink
• Very sick patient
• Comatosed patient
• Severe vomiting

42. • Severe hypernatremia producing:
• Cellular dehydration
• Hyperosmolality in most cases

43. Classification of Hypernatremia
I- Hypernatremia with hypovolemia
II- Hypernatremia with hypervolemia
III- Hypernatremia with euvolemia

44. I-Hypernatremia with hypovolemia
• Causes:
• 1-Renal water loss e.g.
• Osmotic diuretics in excess
• Tubular renal disease
• Adrenal failure
• Impaired response to ADH & DI
– U Na>20 mMol/L
– U Osm<300:400 mOsm/kg water

45. • 2- Non-renal water loss e.g.
• GI loss e.g. diarrhea
• Skin loss, severe sweating
• Peritoneal dialysis
– U Na < 15 mMol/L
– U Osm > 400 mOsm/kg water

46. II-Hypernatremia with hypervolemia
• Causes:
• 1- Iatrogenic (Na containing compounds)
• 2- Mineralocorticoid in excess e.g.
• Aldosteronism
• Cushing disease
• CAH
– U Na >20 mMol/L
– U Osm >300 mOsm/kg water

47. III- Hypernatremia with euvolemia
• Causes:
• 1-Renal water loss e.g.
• DI
• Renal disease
• Diuretics
– U Na variable
– U Osm <290 mOsm/kg water

48. • 2- Non renal water loss e.g.
• Diarrhea
• Fever
– U Na variable
– U Osm > 400 mOsm/kg water

49. Diabetes Insipidus
• I- Central DI
• Idiopathic DI
• Following head trauma
• Neurological disease

50. • 2-Nephrogenic DI
• Sickle cell nephropathy
• Chronic pyelonephritis
• Multiple Myeloma

51. Clinical Features of Hypernatremia
• Neurological features:
– Begin by irritability, to focal deficit up to
cerebral dehydration & hemorrhage
• Cardiovascular features
– Manifestations of volume depletion up to
shock
• Renal features
– Polyuria or oliguria up to renal insufficiency

52. Management of Hypernatremia
• Acute hypernatremia treated rapidly
• While chronic state should be treated
slowly to avoid neurological insults as
seizures and cerebral edema
• Correction should not exceed 2mMol/L/h

53. Management of Hypernatremia:
1- Treatment of the underlying cause
2- Volume repletion with isotonic saline
Hypotonic fluid used after volume repletion
Water deficit replaced over 24 : 48 h
3- Sodium overload :
Removed by loop diuretics & renal dialysis in
severe cases

54. 4- Treatment of DI
- Hormonal replacement (Desmopressin)
- In nephrogenic DI desmopressin is not
completely beneficial but
- Limitation of salt and water intake and
- Thiazide diuretics are the treatment of
choice

55. Potassium

56. Potassium
• Serum potassium (k) range is
3.5 to 5mMol/L
• But 98 % of total body k is intracellular
• Then decrement of 1 mMol of serum
potassium concentration means a loss of
about 200 : 300 mMol/L in body potassium
store.

57. Functions of Potassium
• The main function is the stability of the
action potential of the cell membrane.
• Then the main effect of serum
hypokalemia is hyperpolarization of resting
membrane potential affecting mainly:
• The heart producing arrhythmias and
• The brain affecting the nerve conduction

58. -Potassium also play a role as a cofactor in
enzymatic reactions
-It maintain the normal cell volume
-It affects the IC hydrogen ion concentrations
and participate in regulation of intracellular
PH

59. Hypokalemia

60. Hypokalemia
• Hypokalemia means serum level less than
3.5 mMol/L
• Because potassium is primarily an
intracellular ion, hypokalemia may occur in
low, normal, or high total body potassium.

61. Causes of Hypokalemia
• 1- Redistribution e.g.
–Shift of potassium from ECF to ICF
– Insulin
– Metabolic alkalosis
– Catecholamines e.g. aldosteron
– Periodic paralysis
– Anabolism
– Vitamin B12

62. • 2- Non-renal loss of potassium e.g.
– Gastrointestinal loss mainly diarrhea
and repeated suction
– Discontinued diuretics with alkalosis
– Skin loss

63. 3- Renal loss of potassium
The most common causes e.g.
* Diuretics:
It leads to increase renal tubular flow,
aldosteron secretion & alkalosis
*Aldosteron:
Causing potassium waisting in pressence of
sodium ions

64. * Renal tubular damage:
From nephrotoxin drugs
*Diabetic ketoacidosis:
As a result of osmotic diuresis, and
increased excretion of non-reabsorbable
ketoacid anions.

65. Clinical Effect of Hypokalemia
1- Cardiovascular:
arrhythmias then conduction defects
2- Vascular: postural hypotension
3- Muscular: weakness up to cramps
4- Neurological:
hyporeflexia up to impaired mentation

66. 5- Renal features:
Reduced glomerular filtration to renal
damage
6- Gastrointestinal:
Paralytic ileus, nausea & vomiting
7- Metabolic features:
Glucose intolerance, metabolic alkalosis

67. Management of Hypokalemia
• General measures:
-Treatment of underlying disease
- Correction of other electrolyte
disturbance
-Discontinue offending drug
-Correction of acid base imbalance.
Monitoring for arrhythmias.

68. Potassium Replacement
• Precautions:
• The maximal infusion in 10 : 40 mMol/h
• The minimal concentration given in
peripheral big vessel is 60 mMol/liter fluid
• Potassium should be diluted in nonglucose
solutions
• Avoid over infusion & hyperkalemia

69. Potassium Replacement
• In severe cases i.e. s.k < 2 mMol/L, or
ECG changes or muscle weakness:
• Give up to 40mMol/h in one litter
normal saline iv.
• In mild to moderate cases i.e. s.k >2
mMol/L and no ECG changes:
• Give up to 10mMol/h iv.

70. Hyperkalemia

71. Hyperkalemia
• Hyperkalemia means serum potassium
more than 5 mMol/L
• It may occur with low, normal or elevated
total body potassium stores
• Pseudohyperkalemia results if potassium
is released from cells in the test tube.

72. Most Common Causes of Hyperkalemia
• I- Decreased excretory capacity
• II-Excess intake of potassium
• III- Translocation from ICF to ECF

73. I- Decreased excretory capacity
1- Renal failure when GFR decreases below
10ml/min
2- Potassium sparing diuretics
3- Hypoaldosteronism
4 ACE inhibitors
5- NSAID

74. II-Excess intake of potassium
1- Iatrogenic excess potassium supplement
2- Stored blood
3- Salt substitutes

75. III- Translocation from ICF to ECF
1- Acidosis
2- Severe catabolism & Rabdomyolysis
3- Insulin deficiency
4- Aldosteron antagonists
5- Digitalis toxicity
6-Hyperosmolality

76. Clinical features of Hyperkalemia
* Cardiovascular:
1- Arrhythmias mainly VT & VF
2- Heart block
3- Delayed conduction
4- Ventricular standstill

77. Clinical features of Hyperkalemia
• *Neuromuscular manifestations
1- Paresthesia
2- Muscle weakness
3- Flaccid paralysis
4- Mental confusion

78. Treatment of Hyperkalemia
• General Measures:
– Treatment of underlying disease
– Restriction of exogenous potassium
– Removal of offending drugs

79. Treatment of Hyperkalemia
• Mild Hyperkalemia:
• Restriction of potassium and liberalization
of sodium and water are enough.

80. Treatment of Hyperkalemia
• Severe Hyperkalemia:
1-Calcium 5 mMol IV over 5 min.
2-Sodium Bicarb. 50: 100 mMol over 5min.
3-Loop diuretics
4-Glucose and insulin
5-Hypertonic saline

81. Treatment of Hyperkalemia
6- In resistant cases:
Potassium-binding resins in 50ml
sorbitol 20: 30 g orally/4h
7- Inhaled or infused B2 blocker
8- Dialysis