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WHEN
EVERYTHING IS
NOT O.

Dr Rajesh Kulkarni
B.J.Medical College,Pune
MD,MRCPCH(UK)
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.
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.
CASE 1—CONTD..


ECG:
CASE 1 CONTD..


LAB: Na 131 mEq/L,
K 2 mEq/L



RISK FACTORS FOR HYPOKALEMIA
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.
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
HOW INTRACELLULAR K+ CONTENT
IS MAINTAINED
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
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
SIC WALT
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)
DIAGNOSIS – ETIOLOGY


Due to



Decreased net intake :Uncommon



Shift into cells



Increased net loss



Cause is usually apparent on HISTORY and
physical examination.
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)

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)
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

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

MANAGEMENT


Reduction of potassium losses



Replenishment of potassium stores
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
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?)
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!!!)
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
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)
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
HYPERKALEMIA
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
HYPERKALEMIA

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

Alpha-adrenergic agents(Impairs cellular K+
uptake)



Acidosis (Impairs cellular K+ uptake)



Cell damage (Intracellular K+ release)



Hypoaldosteronism
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).

IS THIS LAB REPORT CORRECT?


Fictitious Hyperkalemia :
hemolysis,
"milking" of extremities ,
thrombocytosis or leucocytosis.
TRUE HYPERKALEMIA
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).
INCREASED K+ INTAKE


Intravenous or oral potassium supplementation.



Packed RBCs (PRBCs)transfusion
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.
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
ECG CHANGES


Tall Peaked T waves (K 6.5)



Prolonged PR, Flat or absent P waves(K 7.5)
ECG CHANGES


Widened QRS (>0.12 Sec) ,



Sine wave pattern(S and T waves merging) (K
8.5)
ECG CHANGES


Bradycardia, Ventricular Tachycardia (K 9.0)
MANAGEMENT


Immediately discontinue any IV potassium
containing fluid/any drugs that may cause
hyperkalemia.
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
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)
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.)
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.
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
C BIG K DROP


C : Calcium Gluconate



B: Bicarbonate



I,G : Insulin and Glucose



K: Kayexelate



D: Diuretics and Dialysis
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+
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.
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.
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
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
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
THANK YOU
ALTERNATIVE APPROACH TO
HYPOKALEMIA


Investigations Required

Urine Potassium
ABG
Urine chloride
Renin/Aldosterone
Hypokalemia and hyperkalemia indore pedicon 2014 final
Hypokalemia and hyperkalemia indore pedicon 2014 final

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Hypokalemia and hyperkalemia indore pedicon 2014 final

  • 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.
  • 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
  • 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)
  • 16.
  • 17.
  • 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
  • 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.
  • 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)
  • 41. MANAGEMENT  Immediately discontinue any IV potassium containing fluid/any drugs that may cause hyperkalemia.
  • 42.
  • 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
  • 44.
  • 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.)
  • 47.
  • 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
  • 57.
  • 59. ALTERNATIVE APPROACH TO HYPOKALEMIA  Investigations Required Urine Potassium ABG Urine chloride Renin/Aldosterone