hypokalemia - pediatric overview, common causes, illustrative figures, pnemonics, easy to understand concepts, practically oriented.

2. OUTLINE
1. INTRODUCTION
2. INTERNAL HOMEOSTASIS
3. ETIOLOGY
4. EXTERNAL HOMEOSTASIS
5. SYMPTOMATOLOGY
6. ECG CHANGES
7. APPROACH
8. TREATMENT
9. REFERENCES

3. INTRODUCTION
• POTASSIUM – most abundant intracellular
cation
• 98% intracellular (100-150 mEq/l) and 2%
extracellular (3- 5.5 mEq/l)
• Ratio of intra- to extracellular potassium
concentration determines, in large part, the
resting membrane potential (RMP)
• critical for normal function of electrically
excitable cells

4. • Goal of healthy human – ZERO potassium
balance
• Requirement 1- 2 mEq/kg through diet.
• About 85% of ingested potassium is absorbed.
• How to maintain 0 potassium balance??
• 90% excreted in urine and 10% in stools and
sweat

5. • robust somatic growth early in life requires
the maintenance - state of positive potassium
balance
• tendency to retain potassium early in
postnatal life is reflected-
higher plasma potassium values in infants and
particularly in preterm neonates.
• Active transport of potassium through
placenta

7. • Only about 50% of ingested potassium is
excreted within 4-6 hrs by kidneys – long term
regulation, rest 40% slowly over weeks.
• How to handle excess potassium present in
diet then ??
• Life threatening hyperkalemia is not generally
observed
• Internal and external mechanisms of
potassium homeostasis

9. •now concentrating
on internal
potassium
homeostasis

10. HOW ??

11. Na – K ATPase channel

12. • Na-K-ATPase transports three sodium ions out
of and two potassium ions into the cell at the
expense of the hydrolysis of adenosine
triphosphate (ATP).
• The unequal cation exchange ratio produces a
charge imbalance across the cell membrane-
electrogenic pump.

13. • Positively charged potassium ions, present in
high concentration within the cell, passively
leak out of cells down a concentration
gradient through ubiquitously expressed
potassium-selective channels.
• A steady state is reached at which the
outward movement of positively charged
potassium is opposed by the negative cell
potential -RMP

14. Neonatology!!
• nonoliguric hyperkalemia- the first 72 h of
life
• serum potassium concentration >7.0 mEq/l, in
the presence of urinary output of >1 ml/kg/h,
despite the intake of negligible amounts of
potassium
• failure of the Na-K pump as well as a limited
secretory capacity of the kidney for potassium
• Prenatal steroid treatment – prevents
nonoliguric hyperkalemia via induction of Na-
K-ATPase activity

15. EFFECT OF ACIDOSIS AND
ALKOLOSIS ON POTASSIUM
• In organic acids – maximum effect
• Reduces activity of ATPase due to reduced
intracellular sodium.
• Abundant protons and depleted bicarb both
contribute

16. • Organic acids – utilize monocarboxylate
transportes and reduce intracellular pH.
Intracellular sodium is maintained by sodium
hydrogen exchanger and sodium bicarb
cotransporter.

18. EFFECT OF INSULIN AND
CATECHOLAMINES ON POTASSIUM
• Insulin causes both insertion of ATPase and
GLUT 4 channels through diverse mechanisms.
• B agonists cause cAMP dependent increase of
ATPase

20. OTHERS - POTASSIUM
EFFLUX
• Hyperosmolality
• Succinyl choline
• Parenteral administration of cationic amino
acids.

21. Case scenario
• 16 yrs old Preethi – admitted last month PICU
• Presented with vomiting, convulsions
• BP- 200/160, hypertensive emergency
• Past history significant with hypertension
diagnosed 1 yr back during appendicectomy
operation.
• Potassium – 1.9
• CT brain – changes suggestive of PRES
• CT angiogram – renal artery stenosis

22. To be continued !!!!

23. ETIOLOGY
• Spurious
• Transcellular shifts
1. Alkalosis
2. Insulin
3. Refeeding syndrome
4. Drugs – barium, HCQ

24. • Decreased intake – anorexia nervosa
• Extrarenal losses
1. Diarrhea
2. Laxatives
3. excessive sweating
4. Kayexalte or clay ingestion

25. Renal losses
Metabollic alkalosis
Hypertension
Cushing syndrome
Renovascular HTN
Monogenic HTN
Normotension
Bartter syndrome
Gitelman syndrome
Diuretics
Without specific acid base
disturbance
Interstitial nephritis
Tubular toxins
Hypomagnesemia
Metabollic acidosis
RTA
DKA
Ureterosigmoidostomy

26. • Spurious
• Decreased intake
• Transcellular shifts
• Increased losses
renal
extrarenal

28. •now understanding
external potassium
homeostasis

31. • PCT - Active Na reabsorption drives net fluid
reabsorption across the proximal tubule, which
in turn, drives K reabsorption through a solvent
drag mechanism.
• Also permissive effect of shift in transepithelial
voltage

33. • TALH - The basolateral Na-K-ATPase pump
maintains intracellular Na low, thus providing
a favorable gradient to drive the apically
located Na-K-2Cl cotransporter.
• The apically located renal outer medullary
(ROMK) channel provides a pathway for K to
recycle from cell to lumen, and ensures an
adequate supply of K to sustain Na-K-Cl2
cotransport

35. • Aldosterone effect on ASDN
• Renovascular hypertension
• Monogenic forms of hypertension

40. Symtomatology of hypokalemia

41. Case scenario
• 3 yrs old Arun – admitted last month in PICU.
• Complaints – generalized edema, loose stools –
15 days
• Lethargic drowsy, tachypneic with shallow
breaths, thready pulse volume, generalized
anasarca and features of malnutrition.
• Investigations showed – dyselectrolytemia
• Potassium – 1.9
• Sodium – 120
• S. albumin – 1.1

42. To be continued !!!!

43. Manifestations
• Cardiovascular
1. Cardiac arrhythmias – sinus bradycardia, PAC,
PVC, junctional beats, ventricular tachycardia,
and AV block.
2. Increased SVR
• Neuromuscular
1. Skeletal muscle weakness
2. Muscle cramps, rhabdomyolysis
3. Smooth muscle dysfunction

44. • Renal
1. Decreased renal conc. ability
2. Decreased Na excretion
3. Increased renal ammonia production
4. Hypokalemic nephropathy- interstitial
fibrosis, tubular atrophy, cysts in medulla

45. • Endocrine and metabolic
1. Negative nitrogen balance
2. Glucose intolerance
3. Decreased aldosterone secretion
4. Hepatic encephalopathy

50. Approach to hypokalemia
• Spurious – no electrocardiographic changes
• History and clinical examination- cause can be
discerned in most cases.
• Diarrhea, vomiting, drug intake, hypertension.

51. • Repeated measurement of blood pressure.
• Concurrent determination of the acid–base
balance, Na+, Cl−, Ca++, Mg++, urea and
creatinine.
• In normotensive subjects, the urinary
potassium/creatinine ratio distinguishes
hypokalemia due to a short-term shift of the ion
into cells (ratio <2.5 mol/mol) from hypokalemia
resulting due to a deficit of the ion(renal losses)

52. • In normotensive subjects with hypokalemia
and metabolic alkalosis, the urinary
chloride/creatinine ratio discriminates renal
from extrarenal (ratio <10 mol/mol) causes

53. Concept of TTKG – difficult

54. • Formula used to assess renal handling of potassium.
• Adjusts the urinary potassium for the concentrating effects
that occur in the collecting tubule, where water is removed
from the urine.
• A high TTKG suggests that the kidney is wasting potassium,
which may be appropriate (in the setting of hyperkalemia) or
inappropriate (in the setting of hypokalemia).
• During hyperkalemia, the TTKG should be greater than 7;
lower values suggest hypoaldosteronism.
• During hypokalemia, the TTKG should be less than 3; greater
values suggest renal potassium wasting.

55. • The safest way to administer potassium is by mouth,
however
• Intestinal conditions that limit intake or absorption of K
• severe hypokalemia (<2.5 mmol/L),
• Characteristic electrocardiogram abnormalities (with or
without cardiac arrhythmias)
• respiratory muscle weakness
• anticipated shift of potassium into cells mandate
intravenous substitution
TREATMENT

56. • Primarily to deal with medical emergencies-
cardiac arrhtymias or resp failure to resp
muscle weakness. Goal is to raise K to more
than 3 mEq/l within 1 – 2 min. Rpt K after 10
min.
• Formula ( 3-measured K) *wt*0.04
(page no. 405 schaeffer)
• Next K is infused @ rate of 0.3 to 0.5
mEq/kg/hr for 2 hrs.
• Stock solution 90 ml NS with 10 ml KCl-
infused @ rate of 1.5 ml/kg/hr for 2 hrs.

57. • In cases of met acidosis with hypokalemia-
treat hypokalemia first.
• In conditions that require IV correction
without acute emergency- double or three
times more K can be added to maintenance
fluids.
• Consider cenrtal line for > 60 mEq/l

58. • Oral route – 2 to 3 mEq/kg/day in 3 divided
doses. Diluted with milk to prevent gastric
irritation.
• Resistant cases of hypokalemia- correct
hypomagnesemia. Reasons - ????

59. Rough guidelines

60. • So how do we treat Arun and Preethi ???
• Both had K < 2.5
• Both did not have cardiac arrhythmias or resp
muscle paralysis
• Hence …….

61. ARUN
• Cause – inadequate intake and malnutrition
• Started on IV potassium correction, 1.5
ml/kg/hr for 2 hrs and then when K levels
more than 2.5, 60 mEq/l given in maintenace
fluids for 48 hrs.
• Then later switched over to oral, given for 14
days as per SAM protocols.

62. • Nutrition – F 75 for 3 days, followed by
transition and F100.
• Edema started to reduce on day 3, discharged
on day 14 after admission.

63. PREETHI
• Cause –renovascular HTN
• IV correction for 12 hrs, later started on oral
potchlor.
• Persistent hypertension- not controlled with 3
antihypertensives.
• Girl was taken up for balloon angioplasty.
• First attempt was failure because of throbosis,
later next attempt given heparin infusion -
successful

64. • Antihypertensives tapered and stopped.
• Electrolytes normal on day 6
• Now BP normal by day 10, discharged

72. REFERENCES
• SCHAEFFER – COMPREHENSIVE PAED
NEPHROLOGY
• AVNER’S PAED NEPHROLOGY
• NELSON 20 EDITION
• BAGGA NEPHROLOGY BOOK
• REGULATION OF POTASSIUM- CJASN EPRESS.
PUBLISHED ON MAY 1, 2014 AS DOI:
10.2215/CJN.08580813
• VIJAYKUMAR AND NAMMALWAR PAED
NEPHROLOGY