POTASSIUM DISTURBANCES,HYPOKALEMIA,HYPERKALEMIA,CHILDREN

1. WHEN
EVERYTHING IS
NOT O.
Dr Rajesh Kulkarni
B.J.Medical College,Pune
MD,MRCPCH(UK)

2. CASE 1
Rahul a 2 year old boy with moderate VSD on Tab
Furosemide 3 mg/kg/day since last 18 months.He had
8 episodes of diarrhea since today morning and was
brought to the ED.
On examination,the pediatric resident noted
“some”dehydration.He also noted abdominal
distension with sluggish bowel sounds.

3. CASE 1 CONTD..
Rahul was started on plan “B” management of
dehydration.(ORS 75 ml/kg over 4 hours)
An ECG was done(for heart disease) and routine
tests including electrolytes were ordered.

4. CASE 1—CONTD..

ECG:

5. CASE 1 CONTD..

LAB: Na 131 mEq/L,
K 2 mEq/L

RISK FACTORS FOR HYPOKALEMIA

6. CASE SCENARIO 2

Vinita is a 7 year old girl, known c/o type 1
diabetes on insulin. She is admitted to the PICU
with Severe DKA and given IV fluids and insulin
as per hospital protocol.

Her initial investigations show K of 4.4 mEq/L
and the on duty resident feels she might get
hyperkalemia if he adds more potassium to the
fluids

After 4 hours she c/o severe weakness and
inability to move her limbs. Her DTR are absent.

7. POTASSIUM

Most abundant cation in human body ,Normal serum
value 3.5 to 5.5 mEq/L.

Regulates intracellular enzyme function and helps to
determine neuromuscular & cardiovascular
tissue excitability.
90 % of total body K+ : Intracellular
( predominantly in muscle )
 10 % : Extracellular fluid


< 1 % : Plasma

8. HOW INTRACELLULAR K+ CONTENT
IS MAINTAINED

9. HYPOKALEMIA
 Defined
mEq/L
as plasma concentration of K+ < 3.5
 Mild
Hypokalemia : 3.0 – 3.5 mEq/L :
asymptomatic
 Hypokalemia
2.5 to 3.0 mEq/L : Moderate, may
be symptomatic
 Hypokalemia
symptomatic
< 2.5 mEq/L : Severe, may be

10. CLINICAL FEATURES

Muscle weakness and flaccid paralysis

Depressed or absent deep-tendon reflexes.


Hypoactive bowel sounds or ileus,constipation
Severe hypokalemia : Bradycardia with
cardiovascular collapse, cardiac arrhythmias and
acute respiratory failure from muscle paralysis

11. SIC WALT

12. FACTORS THAT DECREASE
K+LEVELS

Aldosterone (Increases sodium resorption, and
increases K+ excretion)

Insulin (Stimulates K+ entry into cells by
increasing sodium efflux)

Beta-adrenergic agents(Increases skeletal muscle
uptake of K+ )

Alkalosis (Enhances cellular K+ uptake)

13. DIAGNOSIS – ETIOLOGY

Due to

Decreased net intake :Uncommon

Shift into cells

Increased net loss

Cause is usually apparent on HISTORY and
physical examination.

14. HISTORY
Increased excretion :
Medications (eg, diuretics, antibiotics )
Polyuria
Vomiting or diarrhea
 Shift of potassium into the intracellular space
Recurrent episodes of paralysis
Use of high doses of insulin
High-dose beta-agonist therapy (e.g, for Asthma)


15. WHAT IF CAUSE IS NOT
APPARENT??

Urinary K excretion(spot test)

ABG

TTKG=(Urine K+/Plasma K+) / (Urine Osm/Plasma Osm)
Hypokalemia with extra renal losses,TTKG is
<2
(kidney conserves K+)
Hypokalemia with high TTKG suggests renal
loss
(Not accurate if urine dilute or urine sodium <25 mmol/L)

18. FIRST LINE INVESTIGATIONS
Serum Electrolytes, Urinary Potassium
 ECG
Initially : flattening of t wave
depression of ST Segment
development of prominent u
waves

Severe hypokalemia : increased amplitude of p
wave
increased QRS duration


19. SECOND LINE TESTS
Biochemical tests
Serum renin, aldosterone, and cortisol
24-hour urine aldosterone, cortisol, sodium, and
potassium
Serum anion gap
Drug screen in urine and/or serum
 Hormones
Thyroid Function Tests
 Radiology
Pituitary imaging to evaluate for Cushing syndrome
Adrenal imaging to evaluate for adenoma
Evaluation for renal artery stenosis


20. MANAGEMENT

Reduction of potassium losses

Replenishment of potassium stores

21. REDUCTION OF POTASSIUM LOSSES

Discontinue diuretics/laxatives

Use potassium-sparing diuretics like
spironolactone or amiloride if diuretic therapy is
required (e.g, severe heart failure)

Treat diarrhea or vomiting

22. REPLENISHMENT OF POTASSIUM
STORES

Patients who have mild or moderate hypokalemia
( 2.5-3.5 mEq/L) ;asymptomatic patients:
ORAL THERAPY PREFERRED
POTCHLOR STRENGTH:
20 ml=15 mEq
KESOL 5 ml= 13 mEq
Dose : 0.5-2 mEq/kg PO q12hr
(How to give?)

23. MANAGEMENT
•
In Severe Hypokalemia(Potassium <2) or
symptomatic patients IV Correction
required,
add: 30 meq / L of IV fluid
40 meq / L of IV fluid
50 meq / L of IV fluid
60 meq / L of IV fluid
70 meq / L of IV fluid

ECG monitoring

Frequent testing
I.V.KCL K+ is 2 mEq/ml
(RECHECK!!!)

24. CAUTION!!!
Marked hypokalemia:
Monitor serum K closely
0.5-1 mEq/kg/dose given as an
infusion of 0.5 mEq/kg/hr for 1-2
hour
BOLUS OF KCL I.V. SHOULD NOT
BE GIVEN

25. REVISION—WHICH PATIENTS CAN
HAVE HYPOKALEMIA

Neuromuscular weakness (AFP) esp.if recurrent,
unable to wean off ventilator.

Unexplained abdominal distension,constipation

Children with Asthma , Heart disease and
children on medications that cause polyuria or
loss of K in urine

Children who have rhythm
abnormalities( Bradycardia,hypotension,low
volume pulse)

26. HYPOKALEMIA---TAKE HOME
MESSAGE

Anticipate Hypokalemia in children with
diarrhea,children on diuretics,during treatment
of DKA.

Uncommon causes like Bartter syndrome,RTA
should be considered –look for clues in
history,examination and investigations.

Oral route is safe and effective,IV only if K is less
than 2.5 or symptoms present.

DOUBLE CHECK IV Potassium prescriptions

27. HYPERKALEMIA

28. CASE

A 2 Year old boy was brought to hospital with h/o
loose motions and vomiting since 3 days.

He has not passed urine since 24 hours.

BUN 160 mg/dl ,Creatinine 5.4 mg/dl

Na 123 mEq/L ,K 7.5 mEq/L

29. HYPERKALEMIA
K+ above 5.5 mEq/L,
 Premature infants /young children upto 6.5
mEq/L normal.


30. FACTORS INCREASING K+

Alpha-adrenergic agents(Impairs cellular K+
uptake)

Acidosis (Impairs cellular K+ uptake)

Cell damage (Intracellular K+ release)

Hypoaldosteronism

31. CLINICAL MANIFESTATIONS
Patient may be ASYMPTOMATIC or may have
NONSPECIFIC symptoms or may present with
arrythmia/ CARDIAC ARREST
Respiratory failure and weakness that progresses
to paralysis.
 Nausea, vomiting, and paresthesias (eg,
tingling).


32. IS THIS LAB REPORT CORRECT?

Fictitious Hyperkalemia :
hemolysis,
"milking" of extremities ,
thrombocytosis or leucocytosis.

33. TRUE HYPERKALEMIA

34. DECREASED EXCRETION

Most common cause is Oliguric renal failure.

Other causes include
Primary adrenal disease (e g, Addison
disease, salt-wasting forms of congenital adrenal
hyperplasia),
Hyporeninemic hypoaldosteronism,
Renal tubular disease
(pseudohypoaldosteronism I[or II), or
Medications (e g, ACE inhibitors, angiotensin
II blockers, spironolactone or other potassiumsparing diuretics).

35. INCREASED K+ INTAKE

Intravenous or oral potassium supplementation.

Packed RBCs (PRBCs)transfusion

36. TRANSCELLULAR SHIFTS

Acidosis most common cause

Process that leads to cellular injury or death (eg,
Tumor lysis syndrome, massive hemolysis) can
cause hyperkalemia

Other causes include propofol ("propofol infusion
syndrome"),toxins (digitalis intoxication),
succinylcholine, beta-adrenergic blockade,
strenuous or prolonged exercise, insulin
deficiency, malignant hyperthermia, and
hyperkalemic periodic paralysis.

37. INVESTIGATIONS
FIRST LINE:
 Serum electrolyte tests.
 Serum BUN and creatinine tests
 Urinalysis (UA),ECG,TTKG<6 s/o renal
cause
SELECTED CASES
 ABG,Serum Uric Acid, CPK and calcium
measurements),CBC,Urine electrolytes
 Urine myoglobin test ,Specific drug level
tests for suspected toxicity

38. ECG CHANGES

Tall Peaked T waves (K 6.5)

Prolonged PR, Flat or absent P waves(K 7.5)

39. ECG CHANGES

Widened QRS (>0.12 Sec) ,

Sine wave pattern(S and T waves merging) (K
8.5)

40. ECG CHANGES

Bradycardia, Ventricular Tachycardia (K 9.0)

41. MANAGEMENT

Immediately discontinue any IV potassium
containing fluid/any drugs that may cause
hyperkalemia.

43. STABILIZE MYOCARDIUM

IV Calcium Gluconate (10 %) 0.5 mL/kg IV
over 2-4 min,monitor for bradycardia.May
repeat.Has transient effect.
Indicated in all cases of severe hyperkalemia (ie,
>7 mEq/L), especially when accompanied by ECG
changes

45. SHIFT K INTO CELL

Regular insulin and glucose IV
2ml/kg 50% dextrose (1g/kg) and 0.1units/kg of
regular Insulin over 5-10 minutes (mixed in same
syringe) ,can be repeated after 30 min.
Rapid action,Monitor sugar post insulin

Beta-adrenergic agents, such as salbutamol neb.
2.5-5 mg or Epinephrine (0.05 µg/kg per minute
by intravenous infusion)

46. SHIFT K INTO CELLS CONTD…

Sodium bicarbonate(7.5%) IV
2 cc / kg slowly ,?Efficacy, repetition not
recommended.

A Cochrane review suggests that
Dextrose/Insulin and salbutamol are the first line
therapies most supported by evidence, and that a
combination of
the two therapies may be more effective than
either alone.
(Mahoney BA, et al. Emergency interventions for hyperkalaemia. Cochrane Database Syst Rev
2005;(2):CD003235.)

48. INCREASE K EXCRETION

Loop or thiazide diuretics work well if
kidneys are functioning normally.

Kayexalate(Cation Excange Resin):
exchanges Na for k.
Dose: 1gm/kg/dose every 6 to 8 hrly PO/PR.

49. INCREASE K EXCRETION CONTD..

Hemodialysis
Definitive method ,used in cases of severe
hyperkalaemia or when other treatments have
failed.
K can be lowered by 1-1.5mmol/l for every hour
of dialysis

50. C BIG K DROP

C : Calcium Gluconate

B: Bicarbonate

I,G : Insulin and Glucose

K: Kayexelate

D: Diuretics and Dialysis

51. REVISION—AT RISK CHILDREN FOR
HYPERKALEMIA

Children with low or absent urine output
,hypertension ( ARF)

Children on drugs (K sparing diuretics,ACE
inhibitors)

Children who have rhythm disturbances –always
check K+

52. HYPERKALEMIA-TAKE HOME
MESSAGE

Acute Renal Failure is most common cause of
hyperkalemia.

Uncommon causes like adrenal insufficiency,
aldosterone deficiency should be kept in mind.

Always take hyperkalemia seriously (potentially
fatal).

Calcium gluconate ,Glucose insulin therapy and
salbutamol neb can be lifesaving in
hyperkalemia.

53. REFERENCES

Clinical manifestations and treatment of
hypokalemia .David Mount.Avaialble from
http://www.uptodate.com/contents/clinical-manifestations-and-t
.

Pediatric Hypokalemia Treatment and
Management . Michael J Verive.Available from
http://emedicine.medscape.com/article/907757-treatment.

Mahoney BA, et al. Emergency interventions for
hyperkalaemia. Cochrane Database Syst Rev 2005;
(2):CD003235.

54. CASE HISTORY

A six month old boy was admitted to our hospital
with cough and fever for 4 days, repeated
vomiting and severe dehydration. Within the
past three months he had suffered three similar
episodes warranting hospitalization and IV
fluids, but was normal between episodes and
prior to onset.

Antenatal,perinatal and postnatal period was
uneventful with normal development

On admission, he was in hypovolemic shock with
tachycardia

55. CASE CONTD..

After vigorous fluid resuscitation he was
haemodynamically stabilized. Abdomen,
genitalia and nervous system appeared normal.

His CBC, blood urea, and creatinine were normal
but despite serum sodium being normal
(135meq/l), potassium (2.5meq/l) and chloride
(92meq/l) were low.
His arterial blood gas revealed metabolic
alkalosis with a pH of 7.56

56. CASE CONTD..
His urine electrolytes revealed increased
excretion of sodium, potassium and chloride.
TTKG>4
His subsequent ultrasound scan of abdomen was
normal.

Serum renin was markedly elevated
(11.99ng/ml/hr)
[normal range 0.15-2.33].
DIAGNOSIS

58. THANK YOU

59. ALTERNATIVE APPROACH TO
HYPOKALEMIA

Investigations Required
Urine Potassium
ABG
Urine chloride
Renin/Aldosterone