1. Hypokalemia Dr. Anil kumar.H Assistant professor
Department of pediatrics , BMCRI
CME on fluid and electrolytes , BMCRI , 13/08/2017

2. K Homeostasis
Clinical implications
Etiology
Approach and evaluation
Management

3. Nak ATPase

5. Adults maintain zero potassium balance
Infants and children have positive potassium balance .

6. K Homeostasis
Internal homeostasis
External homeostasis

7. Factors altering K distribution
↑ Uptake
↓ uptake ( shift out )
Insulin
β2 agonists
Alkalosis
Acidosis
Sternous excercise
Hyperosmolality

8. Insulin & β2 agonists

10. Acidosis

11. Alkalosis

12. External homeostasis

14. External homeostasis

15. cv
BS 1
cvv
BS 4
BS 2
cvv b
BS 3

16. The amount of K reabsorbed in the PCT and LOH is a constant fraction of the amount filtered.

17. External homeostasis

18. cv
GITELMAN SYNDROME

19. External homeostasis

21. Determinants of K secretion
Aldosterone
Distal delivery of Na and water

22. Aldosterone Stimulates Na⁺-K⁺-ATPase activity
Increases Na reabsorption
Increases luminal membrane permeability to K

26. Hence , late DCT and CCD plays an important role in K regulation.

28. Clinical implications

29. Functions of K
IC : EC ratio is required for maintaining RMP of cells .
High intracellular K concn. is essential for many cellular processes:
DNA and protein synthesis
Cell growth and apoptosis
Mitochondrial enzyme function
Conservation of cell volume and pH.

30. Cardiovascular effects
Cardiac arrythmias
Premature atrial and ventricular beats
Sinus bradycardia
AV blocks
VT or VF
Increased SVR ( HTN)

33. Neuromuscular disturbances
( Hyperpolarization of muscles and ↓ blood flow to muscles )
Skeletal muscle weakness
Muscle cramps, Rhabdomyolysis
Smooth muscle dysfunction ( GI and urinary system )

34. Renal effects ↓ urinary concentrating ability ( ↓ AQP2 expression )
↑ Renal ammonium production → ↑ HCO3
( Metabolic alkalosis)
Hypokalemic nephropathy ( IF, TA, cyst formation in renal medulla)

35. External homeostasis

36. Endocrine and metabolic effects
Growth retardation
Glucose intolerance
( ↓Insulin release and end organ sensitivity)
↓ Aldosterone release
Hepatic encephalopathy ( susceptible individuals )

38. Etiology

39. Spurious hypokalemia

40. Spurious hypokalemia Metabolically active cells take up K from plasma
No clinical manifestations and ECG is normal
Prevented by immediately separating plasma and storing at 4ºC.

41. 2. Transcellular shifts Insulin Endogenous : Refeeding syndrome
Exogenous : Treatment of DKA
Metabolic alkalosis
β2 agonists
Endogenous: stress, hypothermia
Exogenous : Salbutamol
Hypokalemic periodic paralysis ( recurrent , pptd)

42. Insulin & β2 agonists

43. Alkalosis

44. Total body potassium depleted
Decreased intake
Extrarenal loss ( GI, Sweat)
Renal loss

45. Decreased intake
PEM
Anorexia Nervosa

46. Extrarenal loss
2 yr old child comes with loose stools for 2 days, o/e- severe dehydration
S.E /2.5/117
ABG- Metabolic acidosis
000

47. Average composition of diarrhea
Sodium : 55 meq/l
Potassium : 25 meq/l
Bicarbonate : 15 meq/l
Lower GI loss is associated with acidosis

48. Other causes of lower GI loss
Laxative abuse
K binders

49. 17 yrs old child ( MAY 2017 )
Vomitting – on and off – 2yrs
Abdominal pain , weakness – 6 mths
Had 15 admissions in 2 yrs
P/A: Intestinal loops seen

50. SE- 125/2.5/72
RFT – 127/1.6
ABG :
USG Abdomen- S/o intestinal malrotation with midgut volvulus
RK- 9.8 cms, LK- 8.5 cms
Diffuse ↑ in cortical echogenecity with loss of CMD

51. Average composition of gastric fluid
Sodium - 60 meq/l
Potassium – 10 meq/l
Chloride -90 meq/l
Loss of H+
Upper GI loss- Metabolic alkalosis

53. Other non renal
Cystic fibrosis
Full thickness burns

54. Upper GI loss, ↑ sweat ↓ ECV depletion RAAS activation Hypokalemia

57. Urinary K will not differentiate renal from extrarenal loss

58. Renal loss

59. 4 mths old baby
Not gaining weight since birth
Hurried breathing -2 days
Refusal of feeds days
Birth wt-3 kgs, present wt kgs
Admission at 1 1/2 mths for fever

60. O/E – Dehydrated, Acidotic breathing +
Labs -
ABG : 7/20/356/5.8/-25.3
SE /3.3/131
AG: ( NAGMA)
Urine pH – 7
USG KUB : B/l medullary nephrocalcinosis

61. Diagnosis ?
Distal RTA
Treated with shohls solution and potassium citrate

62. Hypokalemia in RTA In Fanconi syndrome,
Volume depletion leads to RAAS activation.
↑ Na delivery to distal tubules

63. Renal loss with acidosis
Renal tubular acidosis
DKA
Acetazolamide

64. 1 ½ mths female baby ( Nov 2016)
Abd.distension - 2 days
Refusal feeds day
Reduced activity - 1 day
No h/o fever
On EBF , No previous hosp.
FTND, B.wt- 2.1 kgs

65. o/e - lethargic , dehydration +
wt -2.5 kgs
P/A ; Distended, liver 3cm BCM, no FF
Diagnosis : ? Sepsis ??

66. Labs CBC: 10.6/ 12,200/ RFT- 32/0.31 ABG: 7.6/47/221/42.3/+23…. K- 1.3
ECG monitor- inverted T waves, ? U wave
SE: 138/4.2/109

67. Urine Cl meq/L
Urine K – High

68. DIAGNOSIS ?
BARTTERS SYNDROME

69. Subsequent SE…. 30/11 1/12 3/12 4/12 Na 135 138 132 120 127 K 2.3 2
1.9
2.7 Cl 88 86

70. Subsequent ABGs 29/11 30//11 1/12 3/12 8/12 PH 7.6 7.59 7.67 7.56 7.65
HCO3
42.3
46.8
41.8 37 44 BE 23
24.5 21
16.3 26

71. Hypokalemia with metabolic alkalosis with low or normal BP
Bartters syndrome
Gitelmans syndrome
Loop diuretics
Thiazide diuretics

72. cv
BS 1
cvv
BS 4
BS 2
cvv b
BS 3

73. cv
GITELMAN SYNDROME

75. 13 Yr old boy
Presented with headache, photophobia, projectile vomiting and convulsions 4 days back
No h/o fever /neck pain/altered sensorium
No history s/o focal neurologic deficit
No past history of seizures

76. He was evaluated in another hospital, found to be hypertensive – 210/110 mm Hg, treated with labetalol infusion and Inj. phenytoin

77. On examination PR-90/min, BP Rt UL- 150/100 mm Hg Lt UL- 146/100 mm Hg
Rt LL – 150/96 mm Hg
Lt LL /92 mm Hg
No pallor / edema
CNS : HMF- normal
Pupils b/l ERL
No FND
P/A : No renal bruit
No organomegaly

78. Investigations CBC: Hb- 11.8g%, TC-12,150, DC-79/16, PLC-3.4 lac
BU-25, S.Cr-0.8
SE : 131/3/94
Urine – albumin 2+, no RBCs, 8-10 WBCs
ABG : 7.46/41/219/29.2

79. Hypokalemia with metabolic alkalosis with hypertension??

82. Rt Renal artery stenosis

83. Hypokalemia with metabolic alkalosis with HTN
Mineralocorticoid excess

84. With mineralocorticoid excess
Apparent MC excess ( AME )
Gucocorticoid remediable aldosteronism (GRA)
Liddle syndrome
Renovascular HTN

85. LIDDLE SYNDROME
AME

87. Renal loss ( No spcefic AB dist. )
Recovery from AKI
Post obstructive diuresis
Interstitial nephritis
Drugs
Aminoglycosides
Amphotericin –B
Cisplatin

88. Etiology ( summary ) Spurious hypokalemia Decreased intake
Transcellular shifts
Extrarenal loss GI
with acidosis – lower GI loss
with alkalosis - upper GI loss
Skin loss

89. Renal loss With metabolic acidosis- RTA, DKA
With metabolic alkalosis- Bartter , Gitelman syn., loop and thiazide diuretics
No sp. AB abn.- AKI recovery, postobstructive diuresis. Interstitial nephritis
With MC excess - RAS, AME, GRA , Liddle syndrome

91. Approach and evaluation of Hypokalemia

92. Clinical setting usually gives clue :
GI loss
Recovery phase of ATN
DKA
Diuretics

93. ECG… ECG…. Life saving
Repeated BP measurement
ABG
High BP with metabolic alkalosis –
Mineralocorticoid excess

94. Renal potassium handling
Spot urine K > 20 meq/l – abnormal loss
Spot K/Cr ratio - > 13meq/g
FEK- > 6 % is inappropriate response
These differentiate transcellular shifts from K loss, not renal from extrarenal losses.

95. Urine Cl- Hypokalemia and metabolic alkalosis
Differentiates renal from extrarenal losses
Urine Cl- >20 meq/L indicates renal loss

96. PRA and PAC
HTN , Hypokalemia and MA

97. HYOPOKALEMIA(R/O spurious hypokalemia)
Urine K
K/Cr
FEK
Urine K < 20
K/Cr <13
FEK <6
Urine K > 20
K/Cr >13
FEK >6
TC shifts
Diarrhea , burns
Renal loss
Blood pressure
Normal
High
PRA
PAC
M.Alkalosis
M.Acidosis
Urine Cl
RTA
DKA
Acetazolamide
↑PRA
↑PAC
↓PRA
↑PAC
↓PRA
↓PAC
Low < 20 meq/L
Vomitting CF
High > 20 meq/L BS GS
Diuretics
RAS
RST
GRA
Adrenal adenoma
Liddle
AME
CAH

99. Management IV supplementation is indicated in:
Symptomatic patients with severe hypokalemia (< 2.5meq/L)
ECG abnormalities
Respiratory muscle weakness

100. Aim is to increase serum K to > 3 meq/L in 1-2 mins
( 3-obs. K ) x BW x 0.04
Rate of infusion should be meq/kg/hr

101. In transcellular shifts
0.5-1meq/kg/dose of Kcl is given over 1-2 hrs
Infusion rate should not exceed 1 meq/kg/hr
Concn. Should not exceed 60meq/l
( peripheral) and 80meq/l in central line .

102. Should not be mixed with dextrose solution
Hypokalemia should be corrected before correction of acidosis.

103. In c/c hypokalemia , as in BS, IC:EC ratio is maintained at the cost of TB K wasting
Oral potassium can be given
Potassium chloride is preferred.

104. In RTA , oral potassium can be started
Correct potassium before correction of acidosis
Potassium citrate is preferred .

105. Overcorrection can lead to hyperkalemia , particularly in transcellular shifts
Should be given under ECG monitoring

106. Potassium preparations
Parenteral KCl solution ml = 2meq K Oral KCl ( potklor ) ml = 20 meq Oral K citrate ( potrate ) 1 ml = 2 meq K Potassium phosphate ( DKA ) , not available freely .

107. Other drugs in specific situations
Indomethacin – Bartters syndrome
Amiloride Liddles syndrome
Spironolactone

108. Key messages Most of the times there is a clue to etiology
Causes - Transcellular shifts, renal and Extrarenal losses
ECG when u suspect hypokalemia
Check BP and ABG in all cases of hypokalemia
Urine K+ does not differentiate renal from extrarenal loss
Urine Cl- helps in differentiating renal from extrarenal cause

109. Oral K supplementation is safer except in life threatening situations
Potassium chloride – alkalosis
Potassium citrate – acidosis