This document discusses dyselectrolytemias (fluid and electrolyte disturbances) that commonly occur in intensive care units. It covers several key points: - Fluid and electrolyte disturbances are among the most common clinical problems in ICU patients and increase morbidity and mortality. Disturbances can involve sodium, potassium, chloride, calcium, phosphate, and magnesium. - Critical illnesses like trauma, sepsis, brain damage and heart failure can disrupt fluid and electrolyte homeostasis through mechanisms like reduced kidney perfusion, activation of hormones, and renal tubular damage. Inappropriate fluid/electrolyte administration is also important. - Hypo- and hypernatremia are independent risk factors for poor prognosis in ICU

1. Dyselectrolytemias in Intensive
Care Unit
Dr Vilas Naik
DM (Nephrology)
Fellowship in Nephrology (University of
Toronto)

2. Fluid and electrolyte disturbances
• Most common clinical problems encountered in the
intensive care unit (ICU).
• Increased morbidity and mortality among critically ill
patients.
• Disturbances of monovalent ions (Na, K, Cl) and divalent
ions (Ca, PO4 and Mg)
• K, Mg and PO4 are mostly intracellular cations.Cl exists
in the extracellular space, at electrochemical equilibrium
with Na.
Electrolyte blood press
V8 (2);dec 2010

3. Fluid and electrolyte disturbances
• An alteration in this ratio: significant effects on acid base
balance
• Critical disorders like trauma, sepsis, brain damage, and
heart failure cause disturbances in fluid and electrolyte
homeostasis.
• Mechanisms: reduced perfusion to the kidney
(hypovolemia or hypotension), activation of hormonal
systems such as RAAS and AVP, Renal tubular damage.
• Most important: inappropriate administration of fluid and
electrolytes

4. Fluid and electrolyte disturbances
• Formulae to guide the therapy:
– All formulae regard the patient as a closed system
– none takes into account ongoing fluid losses that are
highly variable between patients
– Therapy must be closely monitored with serial serum
and urine electrolyte measurements.
Semin Dial. 2006 Nov-Dec;19(6):496-501.

5. Dysnatremias
• Prevalence 20-30% in some studies
• hypo- and hypernatremia in ICU, independent
risk factors for poor prognosis
• Disorders of water balance
• Often iatrogenic
Can J Anaesth 2010 Jul;57(7):650-8

6. Hyponatremia

7. Hyponatremia
• Commonest electrolyte disorder in
hospitalized patients
• Mostly iatrogenic- wrong fluids, surgical
wards and postoperative patients
• concept of “maintenance fluids”

8. Overview
• Definition
• Physiology of Na and H2O
• Case
• Classify
• How urgent is the treatment and whom to treat?
• Treatment guideline.

9. Hyponatremia- Define it
• Relative water excess
Sr Na < 136 Meq/ L
– Low water and lower sodium content in the body
Hypovolemic hyponatremia
Extracellular fluid volume contraction (true volume depletion)
Syndrome of appropriate ADH secretion

10. always water excess

11. Hyponatremia- Define it
– Normal or excess Na, and still higher H2O content
CHF, Nephrotic syndrome, cirrhosis of Liver
Non osmotic release of ADH
“Effective” circulating volume contraction

12. Always relative excess of water
1L, 140 Na
2L, 200 Na
140 Meq/L 200Meq/L

13. Don’t forget ADH…..
• Water surplus/ excess alone….
– Excess free water (electrolyte free water) ingestion alone –
will result in large quantity of maximally diluted urine
– So only water surplus – cannot cause/ sustain hyponatremia
– ADH – almost always present
– What we want to know is why is the ADH present?

14. Symptoms and signs
of hyponatremia
• None
• Headache
• Lethargy
• Dizziness and ataxia
• Mild confusion
• Psychosis
• Seizures
• Coma

15. Salt and water physiology

16. In an adult female and male- water content of
the body (TBW) is approximate 60% and 50%
of body weight
2/3—1/3

17. ADH physiology
Water reabsorbtion
Or
Water loss ADH

18. Osmoregulation Volume regulation
What is being
sensed
osmolality Effective circulating
volume
Sensors Hypothalamic
osmoreceptors
Carotid sinus,
Atria
Aff. Glomerular arteriole
Effectors ADH Sympathetic NS
RAAS
Natrauretic peptides
ADH
What is being
effected
water excretion
(ADH) Sodium excretion
H2O intake (thirst)

19. ADH and Sr Osmolality
Osmolality varies within 1%
282
varies

20. ADH and blood volume
SNS
RAAS
ADH
5%
8%
12-15%

21. ADH physiology

22. ⇑ OSM or ⇓ Volume….. ⇑ ADH

23. Reverse is the true
⇓ OSM or ⇑ Volume…..⇓ ADH

24. ADH disorder…Na disorders

25. ADH acts on medullary collecting ducts (aquaporin
type 2 receptors) - inserts Aquaporin (water) channels:
very rapid reabsorption of water

26. Filtrate/ water reabsorption
86 % water
H2O
impermiable
CCD & MCD
H2O permiable

27. Endocrine factors-Hypothyroidism
• Hypothyroidism
– commonest electrolyte derangement in hypothyroid
– Hyponatremia : 45% of hypothyroid patients
– Increased serum creatinine
– Decreased glomerular filtration
– Decreased sodium reabsorption
⇓renal ability to dilute urine- water excretion
So a very much
Correctable factor
that can lead to
hyponatremia

28. Endocrine factors- Addisions disease
• Pigmentation
• salt craving
• hypotension
• hyperkalemia
• hypersecretion of ADH:
– reductions in BP and cardiac
output
– salt wasting with resultant
volume depletion
– Hypovolemia stimulates the
release of ADH
– Hyponatremia corrected by
cortisol and volume repletion,
shuts off ADH release.

29. Case 1
• 66 yrs old lady, HT since 5yrs
• 1 month ago: BP- 160/94, thiazide added to amlodep
• Progressive lethargy, fatigue, only taking liquids
since 5 days. c/o decreased urine output.
• Confused since 1 day- GTCs 1 hr ago
• Hospitalized: 60 kg (previously recorded)
– HR- 100, BP 130/70, low JVP, post ictal state.
– Appeared volume depleted

30. Case 1
• Treatment:
– Catheterized- 200 ml immediately removed,
blood tests sent, IV access, Ryles tube
– FPBS- 106, IV NS 1000 ml over 1/2 hr
– Noted urobag to be full- staff assumed retention,
everyone happy.

31. We got the blood tests…..and I was worried
Parameters Blood urine
Na 125 8
K 3 10
Cl 62 12
Total protein 8.4
Hb / Hematocrit 17 gm/ 51%
HCO3 30
Urea 55
Creatinine 1.6
Ca 9.5

32. Case 1
more worried when diuresis occurred
and Na changed rapidly
Repeat Sr Na, exactly 2 hours later
135 Meq/L
Urine output was 2L in 2 hours

33. Case 1
• Why did this happen?
• Risks?
• What went wrong?
• What do we do next?

34. Case 1- why did this happen
• Lets calculate what went in and how much should have the
Sr Na changed.
– TBW= 30 L (50% of weight in females)
– Given 150 Meq/ L of 0.9 % NS (ie 1 L of H2O + 150 Na)
– Na deficit (Na to be replaced to achieve a particular Sr Na
Level) = TBW (desired Na- actual Na)
– 150 Meq/L = 31 L (x- 125 Meq/L).
– “X” is what the Na should be, if we replace 1 L of 0.9% NS
– X = 5 Meq/ L

35. Why did this happen ?
• ADH shut off- volume
replacement
• Free water diuresis-
– Electrolyte free water is
excreted
– So if H2O is removed from
body, Na concentration
rapidly increases

36. Risks
• Osmotic demyelination
syndrome (ODS or CPM)
– Under estimated incidence
– Critically ill ICU patients,
difficult to diagnose
pons
Non pontine areas

37. Pathogenesis and clinical features
• Chronic hyponatremia-
brain cell adaptation
– Lose osmolytes & H2O
– Protection against cerebral
edema
• Rapid correction- no time
for adaptation
– Brain cells shrink- apoptosis
• Symptoms
MRI changes are
Late.
Mimics any other diffuse
Encephalopathy.
Brain
edema
adaptation

38. What went wrong?
• Classify hyponatremia
– Acute Vs Chronic is the only useful one for treatment
– Most chronics have an acute component
– In our case, even before we classified it, we corrected it
inadvertently
– Lady definitely had and acute component, excessive water
drinking….
• Why did the Na correct so rapidly even with 150 Meq/L
of Na?

39. What went wrong?
Why did the Na correct so rapidly?
Thinking beyond the algorithm for Na correction
• 1 L of 0.9 % NS (150 Meq/L of Na)- the Sr Na
should ⇑ by 5 Meq/ L
• Why did it go up so rapidly?
The concept of tonicity balance
What goes in and what comes out?

40. Tonicity balance
Input
1 L NS
i.e. 1 L of H2O
+ 150 Meq (Mmols)
Of Na
Body compartment
Na and water Content
Output
2 L urine
U Na + K = 40
i.e. 2 L of water
And 40 mol Na +K
30 L TBW in 60kg female
30 L of water
3750 Mmols Na

41. Tonicity balance- new body content
of Na and water
Body compartment
New Na and water Content
30 L TBW in 60kg female
Water= 30+1-2=
29L
Na: 3750+ 150-40
3910
Sr Na = 3910/ 29
134.8
And that was
Our Sr Na after
2 hours

42. Why GTCs at Na of 125??
• 1st
- we check Venous Na, not arterial.
– Brain sees arterial Na, not venous.
– Arterial Na 3-5 Meq/L lower than venous Na
• 2nd
and more important-
– Post GTCs: seizures increase Sr Na!!!
– During seizures, muscle cells produce osmotically
effective molecules
– So water shifts in muscle cell- Sr Na can rise by 10 to 15
Meq/L after seizures

43. Don’t forget the water in GI tract..
• Most cases of acute on chronic hyponatremia,
occurring at home- solute free water intake/
fruit juices etc – water source
• Insert RT in hyponatremic convulsion-
remove water in stomach if its there

44. Remember about K correction….
• Most body K – intracellular
• K replaced for correction of hypokalemia:
– Enters the cells, intracellular Na comes out
– So giving 80 Meq/L of K is equivalent to giving
Na
– K replacement is equivalent to giving Na

45. Back to our Case
• Lower the Na: 1 L of 5D = will decrease Na by 5Meq/L
– 3910/30= 130
• Stop further diuresis of free water: DDAVD
(desmopressin)
– Ideally IV 2 to 10ug, till urine output < 100 ml/hr
– Used 20 ug intranasal- decreased diuresis
• 6 hrly monitoring of Sr and urine electrolytes
• Replace what comes out (urine)- volume + electrolytes

46. Replace what comes out (urine)
• Urine 100 ml/ hr, Urinary Na + K = 70
– Give half NS with Na content of 75 meq
– This will prevent further rise
• Urine Na + K 40 Meq/ L
– 500 ml 5D + 500 ml 0.45 NS = 37 Meq/ L of Na
• Free water restriction to < 1 L/ day
• Oral K replacement, isotonic fluid of KCL if IV

47. Case 2
• 37/F, No significant past history
• DUB- advised hysterectomy.
• Low risk, pre-op investigations- WNL
• Cardiac evaluation – normal
• Surgery under SA, lowest intra-op BP- 100/60

48. Case 2
• Received 1L RL (Na- 130 +4 K) intra-op, post-
op: 1000 ml of 5% D and 500ml of NS over
3hs.
• GTCs
– CBC, Sr Ca, Sr Mg all normal
– Na- 125
Why did the lady develop hyponatremia acutely?

49. Case 2
• Urine output- 1.5 L once she was catheterised,
till she convulsed.
• Urinary Na- 190, K- 60

50. Tonicity balance
50 kg lady
Input
2.5 L
i.e. 2.5 L of H2O
+ 210 Meq (Mmols)
Of Na
Body compartment
Na and water Content
Output
1.5 L urine
U Na + K = 250
i.e. 1.5 L of water
And 375 mol Na +K
25 L TBW in 50kg female
25 L of water
3500 Mmols Na

51. Tonicity balance- new body content
of Na and water
Body compartment
New Na and water Content
25 L TBW in 50kg female
Water= 25+2.5-1.5=
26 L
Na: 3500+ 210-
375
=3335
Sr Na =3335 /26
127
And that was
Our Sr Na

52. Why hyponatremia?
• Obviously ADH was on board……..
• Where did it come from.??
• Pain & nausea are very powerful stimulants…

53. Why convulsions at 125?
• Young female, small muscle size
• Acute hyponatremia..
• Treatment
– 3% 200 ml to acutely raise the Sr Na by say 5
Meq/L
– Then correct the remaining over next 24 hours
– Relief of nausea and pain will help correct ⇓ Na

54. Summary of guidelines for therapy
• Classify acute Vs Chronic- history, change in
medications
• Assess volume status
– Most reliable hematocrit and total Sr. proteins
– Urine electrolytes (UNa < 10)
– Hemodynamic and clinical: least reliable
• Therapeutic considerations in acute hyponatremia and
diagnostic considerations in chronic hyponatremia

55. Summary of guidelines for therapy
• Acute component of Chronic:
– Raise Na by < 5 Meq/L, use 3% NS
– Later fluid restriction and find the cause
• Ask 2 questions in the patient with low Na
– Why is the ADH present?
– Will the release of ADH cease and cause rapid
water diuresis?

56. Copyright ©2006 American College of Cardiology Foundation. Restrictions may apply.
deGoma, E. M. et al. J Am Coll Cardiol 2006;48:2397-2409
Vasopressin (AVP) stimulates synthesis of aquaporin-2 (AQP) water channel proteins and
their transport to the apical surface of collecting duct principal cells

57. • Symptoms
• of hyponatremia may not be apparent in
ventilated and
• sedated patients in the ICU, and worsening
of cerebral
• edema may lead to catastrophic
consequences such as
• brainstem herniation and respiratory arrest.

58. Hyperkalemia

59. Hyperkalemia: Life threatening Emergency
Common
Treatable

60. K physiology
• Total body K stores are approximately 3000 meq
• K: primarily intracellular cation {98 % of body K}
• Ratio of the K concentrations in the cells and outside:
major determinant of the resting membrane potential
across the cell membrane
• Generation of the action potential: essential for normal
neural and muscle function
• K abnormalities: Muscle weakness and arrythmia

61. Regulation of urinary potassium excretion
Connecting segment & Cortical duct
Na comes here
Lumen
Negative
ROMK
Electrical gradient
For K secretion
Na-K ATPase
Electrical and
chemical
gradient for Na
reasbsorption

62. Regulation of urinary potassium excretion
Stimulation of K secretion by principal cells
• An increase in plasma potassium
concentration and/or potassium intake
• An increase in aldosterone secretion
• Enhanced delivery of sodium and water to
the distal potassium secretory site

63. An increase in plasma potassium
concentration and/or potassium intake

64. An increase in aldosterone secretion
Hyperkalemia
Renin angiotensin
Aldosterone system
(RAAS)
Na channel
Aldosterone deficiency,
blockade

65. Enhanced delivery of sodium and water
to the distal potassium secretory site
We need Na and
Water here.
No distal Na (decresed GFR),
No K secretion
e.g Renal failure
Increased distal flow,
Increased Na delivary,
Increased K secretion
Eg diuretics

66. Distribution of potassium between the
cells and the extracellular fluid
98 % K intracellular
Maintained by this
pump
Pump block
eg digitalis toxicity
Beta blockers
Pump stimulation
Insulin, beta2 stimulation

67. Distribution of potassium between the
cells and the extracellular fluid

68. Distribution of potassium between the
cells and the extracellular fluid

69. Hyperkalemia
• Increased intake: K adaptation, rapid
• Shift: intracellular to extracellular, alone again not
enough to sustain hyper K.
• Decrease excretion: almost always present
– Aldosterone
– Decreased distal delivery of Na/ water
– Renal dysfunction

70. Case 1
• 52/ male, DM and HT- 15 yrs
• Uncontrolled HT, Edema 3+
• Recent change in medications
• Adm: rapid onset quadriparesis over last 24
hours

71. Case1: examination
• ECG: HR of 30, broad QRS, CHB like pattern
• Rest vitals stable
• Higher functions normal
• Quadriparesis (grade 2 power, absent reflexes)

72. Case 1: Labs
• Na 129
• K 8.7
• Cl 96
• HCO3 16
• AG 17
• Creat 4.4
• Glucose 600
• CBC leucocytosis
• Urine
• Sugar- 4+
• Ketones- nil
• Plenty pus cells

73. Hyperkalemia appraoch
• Intake
• Shift
• Impaired excretion

74. Case: analysis
• Intake: propably reduced (UTI, blood sugars)
• Shift:
– Severe hyperglycemia
– Insulin deficiency
– Acidosis

75. Case analysis
• Decreased renal excretion (almost always)
• Was started on ramipril (ACEI) for HT
– RAAS blockade (decreased aldosterone)
Decreased GFR
so decreased distal delivery of Na and water,
no Na reabsorption, no electronegative potential in lumen
No secretion of K

76. Na+
--
--
--
--
--
K+

77. Case analysis
• The patient was also
started on
spironolactone which
blocked aldosterone
action
• NSAIDS for fever
– Deceased GFR
– Renal failure

78. More mechanisms
• K loading increases ROMK expression and insertion into
CCD luminal membrane
• ? May be gut signal to kidney to change ROMK
• Another K channel in CCD
– High capacity K channels (big K or Maxi K)
– Activated of high flow (water and Na delivery)
– Activated by K depletion
– Aldosterone independent action

79. Another K channel: intercalated cells
• H-K exchanger in IC
cells of CCD
• Activated in K depletion
• Absorbs K+ and
secretion of H+

80. Evaluation of hyperkalemia
• Exclude Pseudohyperkalemia
– potassium movement out of the cells during or after
the blood collection
– Torniquet
– Thrombocytosis, high WBC counts (leukemias)

81. Assessing K excretion
• Kidneys can vary K excretion from < 5 Meq/L to 400
Meq/L, with decreased or increased intake
• Urine K/ Creatinine ratio
– < 15 mmol/gm in K depletion
– >200 mmol/gm in hyperkalemia
–

82. Case 1
• Urine Na- 120 Meq/L
• Urine K- 15 Meq/L
• SO distal delivery of Na is adequate
• Severely impaired K excretion
• Aldosterone deficiency: hyporeninemic
hypoaldosteronism in DM
• Drugs blocking aldosterone production and action
• Decreased GFR

83. Case 1
• NSAIDS: worsening of RFT (GFR)
• PG synthesis inhibited
– PG inhibit renin –reduce aldosterone
• So in this patients, almost all things to increase
his K has been done
– ACEI, aldosterone blockade
– NSAIDS

84. Treatment of severe hyperkalemia
• Calcium: if hypocalcemia or ECG changes
• Shift inside the cells:
– Insulin alone (hyperglycemia) or with 25 %
– Dextrose
– B2 agonist
– Bicarbonate if acidosis

85. Treatment
• Excretion
– Saline, especially if depleted
– Thiazide and loop diuretic
– K binding resins, small effect, increasing GI
excretion, given with lactulose
• Dialysis- the most rapid and effective means in the
presence of renal dysfuction and fluid overload

86. Case 1
• We started the patient on dialysis, normal
sinus rhythem in 45 minutes
• Stopped implicated drugs, treated UTI
• Baseline creatinine of 2 mg % on follow up.
• K normal

87. The message..
• Increase intake- not sufficient
• Hyperkalemia is always a kidney problem
• Consider shift
• Drug history very important
• Assess excretion
– Urine electrolytes- distal Na delivery
– Aldosterone deficiency/ block
– Urine K/ Creatinine is important

88. Hypokalemia

89. Severe K
Emergency
Arrythmias
Muscular weakness

90. In ICUs….
• Upto 20% of patients
• Symptoms: mainly neuromuscular
• Risks:
– Respiratory muscle weakness, difficult to wean
– Life threatening cardiac arrthymias
– Paralytic ileus, risk of transmigration, nutrition

91. hypokalemia
• Low intake: possible, if prolonged, critically ill
– Kidneys can decrease excretion < 20 Meq/ day
– Low intake alone, not be sufficient unless severe
• Shift very important in this settings, drugs
• Excretion: diuretics
– Drugs like amphoterecin B
– Non absorbable anions- penicillins

92. Case 1
• 62/F, diabetic- 10 yrs, HT
• Admitted with fever, cough, SOB: 8 days
• Pneumonia
• Anorexia, severe nausea
• Meds- insulin, amlodepine, thiazides
• HR- 130, BP- 766/50, volume depleted

93. Case 1
• Hb- 14, TLC- 26000
• Creatinine- 1.2 mg%
• Na- 130, K- 4.6, Cl- 96
• HCO3- 23, pH- 7.3
• BS- 600

94. Case 1
• CAP: levofloxacin, pipericillin- Tazobactum
• IV insulin 20 units bolus, Insulin drip
• IV NS 1 L bolus, another 1 L after an hour
• BP 80/50
• Dopamine drip
• 6 am, inablility to move limbs
• Intubated because of hypoventilation, hypoxia

95. Case 1
• Na- 134, K- 1.8, Cl-102
• Urine output- 1200 ml
• Urine K- 20 Meq/L, Na - 12
Where did the K go?

96. Case analysis
• Intake- poor, nausea
– Likely lower body content: thiazides
– Hyperglycemia (sepsis)- osmotic diuresis
• Initial K normal: shift out of cells
– Hyperglycemia
– Insulin deficiency

97. Case analysis
Shift
insulin
Beta stimulation
Endogenous
Salbutamol
Dopamine/dobut
Alkalosis
Bicarb infusion

98. Shift
• Increased RBC production:
– treatment of megaloblastic anemia with B12 or folic
– GMCSF for neutropenia
• Hypokalemic periordic paralysis: Ca channel mutation
• Thyrotoxic paralysis
– B2 receptor stimulation
– Insulin resistence hyperinsulinemia

99. Shift
• Chloroquin intoxication
• Anti phychotic drugs: quitiapine and
resperidone

100. Case analysis: Renal excretion
• Distal delivery of Na and K: NS infusion
• Diuretics: increase distal delivery of Na and
Water
• Hyperglycemia: Osmotic diuresis

101. Excretion: Distal delivery of Na
Na comes here
Lumen
Negative
ROMK
Electrical gradient
For K secretion

102. Renal excretion: aldosterone
• Aldosterone: Stimulate ENAC, Na-K- ATPase
– Malignant Hypertension: RAAS, Symp Nervous
system stimulation
– Primary aldosteronism
– Endogenous and exogenous Steroids :
Action on mineralocorticoid receptors

103. Renal excretion: aldosterone

104. Renal excretion: non-reabsorbable anions
• Like β-hydroxybutyrate in DKA,
– penicillin derivative in high dose penicillin therapy
• Accompanying Na ions, increased distal delivery, more Na
reabsorption, more lumen negative
• Final pathway here is increased distal Na delivery

105. Renal losses
• Renal tubular acidosis
• Hypomagnesemia
• Barrters and Gietelmanns syndrome

106. Extra renal loses
• Loss of gastric secretions (vomiting, aspiration)
– Little K in gastric juice
– Loss of H+ met alkalosis increased HCO3 + Na
– Na exchanged with K
• Diarrhea: K content in intestinal juices (30- 50 meq)
•

107. Case analysis
• Decreased intake- yes, low stores (thiazides)
• Shift: definitely
– Insulin
– Beta stimulation
• Excretion: NO. Urine Na and K,
appropriately low