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Hyperkalemia management
Dr.Khalid Hama salih
Ass.prof of Pediatrics
M.B.Ch. D. C.H F.I.B.M.S.ped
University of sulaimany
College of medicine
Pediatrics department
DEFINITION
It is defined as a serum potassium
concentration greater than 5.5mEq/L
The normal serum concentration range for
potassium is 3.5-5.0mEq/L
 The incidence of hyperkalemia in the pediatric population is unknown, but is considered
rare.[7] However, the prevalence of hyperkalemia in extremely low birth weight premature infants
can exceed 50%.
 The incidence in hospitalized patients ranges from 1% to 10%, and mortality
amounts up to 1 per 1000.
It can be classified according to
severity
Mild hyperkalemia-5.5_ 6mEq/L
Moderate hyperkalemia-6.1-6.9mEq/L
Severe hyperkalemia->7
Causes
K
major mechanisms of
true hyperkalemia are
Pseudohyperkalemia, usually
due to hemolysis of the blood
specimen, is the most likely
cause of an elevated serum or
plasma potassium level in
children. Other Leukocytosis
or thrombocytosis
A.Increased
potassium intake
B.Tubular
unresponsevines
to aldosterone
C.Redistribution
of potassium into
extracellular
D.Reduced
urinary potassium
excretion
Increased potassium release from
cells, most commonly due to (eg, ,
prolonged seizure, hyperthermia, o
exercise), tumor lysis syndrome,
massive transfusion, and metabolic
acidosis,HYPEROSMOLALITY:
(Hypertonic
dextrose,Mannitol,iv
immunoglobulins )
Medication
Eg. NSAID, trimethoprim,
heparin, chemotherapy, K-
sparing diuretic, ACE
inhibitor, beta blockers,
succinylcholine, digoxin,
mannitol
CLINICAL PRESENTATION OF
HYPERKALEMIA
GENERAL
• Related to the effects of excessive k+ on neuromuscular, cardiac
& smooth muscle cell function
Clinical features
• Serum potassium level 5 to 7 mEq/L: Generally asymptomatic
• Serum potassium level greater than 7 mEq/L: Muscle weakness,
paralysis, and cardiac changes on electrocardiography and
arrhythmias. Sudden arrest may occur.
SYMPTOM
• Frequently asymptomatic however patient may complains of
 Dyspnea .palipitation.
 Nausea or Vomiting Chest pain
Laboratory evaluation
•Laboratory tests are based upon probable etiology. All patients with true
hyperkalemia should have the following tests obtained:
•Blood urea nitrogen (BUN)
•Creatinine
•Blood glucose
•Serum electrolytes
•Urinalysis
•Urine electrolytes
•where adrenal insufficiency is suspected, additional testing includes:Serum
cortisol and ACTH (prior to administration of exogenous corticosteroids)
Copyrights apply
Peaked T waves of Hyperkalemia. Note the
amplitude of the T exceeds the amplitude of
the R. Care of Life in The Fast Lane blog
Example of bradycardia with absent or
flattened p waves in hyperkalemia
Management
Management
1.Stop all potassium intake
• 4.Remove
potassium;
2.Stabilize cardiac
membranes with calcium
3.Transe cellular shift
calicium :Give only for 1.ECG findings (eg, widening of the QRS complex or loss of P
waves, but not peaked T waves alone) or 2.severe arrhythmias thought to be caused by
hyperkalemia or in patients with 3. a potassium level ≥7 mEq/L.
•For perfusing patients, give calcium gluconate 10% solution 60 mg/kg; given as 0.6
mL/kg diluted in an equal volume of D5W or NS, maximum 2 g (20 mL, 4.5 mmol) per
dose IV or IO over 5 minutes. Time to onset of action is immediate. May repeat in 10
minutes as needed for persistent ECG changes or arrhythmias.
¶
•For cardiac arrest, give calcium chloride 10% solution 20 mg/kg given as 0.2 mL/kg,
maximum 2 g (20 mL, 14 mmol) per dose; dilute in an equal amount of D5W or NS and
give slow IV via central venous access or IO push; repeat in 10 minutes as needed for
persistent arrest, ECG changes, or arrhythmias.
Δ
Insulin and glucose:
Onset of action is 10 to 20 minutes. Only give if significant ECG
changes or confirmed serum potassium ≥7 mEq/L.
Give regular insulin (dose of 0.1 units per kg, maximum dose of 10 units) along with
dextrose (glucose) dose of 0.5 g/kg over 30 minutes. The administration of dextrose
is based upon the age of the patient as follows:Children younger than 5 years of age:
Give 10% dextrose (100 mg/mL) at a dose of 5 mL/kgChildren 5 years of age and
older: Give 25% dextrose (250 mg/mL) at a dose of 2 mL/kg.
For patients with :
a.severe acute symptoms. b.ECG changes, c.arrhythmias, d.impending arrest
Larger doses of regular insulin (0.2 units/kg) and dextrose (1 g/kg, 10 mL/kg of 10%
dextrose or 4 mL/kg of 25% dextrose) can be administered.
Repeat dosing can be given after 30 minutes if needed.
The major adverse effect is hypoglycemia, and serum glucose level should be
monitored closely and additional dextrose administered as needed.
Beta-2 agonist: Onset of action is 20 to 30 minutes.
Give nebulized albuterol (salbutamol) with dosing based upon patient weight as follows:
Neonates: 0.4 mg in 2 mL of saline
Infants and small children <25 kg: 2.5 mg in 2 mL of saline
Children between 25 and 50 kg: 5 mg in 2 mL of saline
Older children and adolescents >50 kg: 10 mg in 2 to 4 mL of saline (doses up to 20 mg have been used)
Inhalation may be repeated after 20 minutes. Inhaled albuterol may also be administered by metered dose
inhaler (MDI) as 4 to 8 puffs with spacer.
Pitfall: If B-agonists are given before insulin/glucose they may cause a transient rise in the serum
potassium level. Always give B-agonists after insulin/glucose.
Sodium bicarbonate:
Onset of action is 15 minutes. Provides minimal effect on shifting potassium intracellularly and
should not be the only therapy used in the management of hyperkalemia, even in acidotic children.
Give 1 mEq/kg (1 mmol/kg). Maximum single dose of 50 mEq (50 mmol) which can be provided as 1
mL/kg of 8.4% solution or, for children less than 6 months of age 2 mL/kg of 4.2% solution administered
over 10 to 15 minutes.
A repeat dose may be given 10 to 15 minutes after last administration. Do not give in the same IV line as
calcium because of a risk of precipitation.
since the effect of above therapies is transient, treatments to remove potassium are
also required:
Loop diuretic: Provides only limited short-term effect. Give furosemide 1 mg/kg higher
dose may be required with renal insufficiency; fluid losses must be replaced unless the
patient is volume expanded. The onset of effect is 1 to 2 hours. May be repeated after 6
hours.
Cation exchange resin (sodium polystyrene sulfonate): Give sodium polystyrene
sulfonate (without sorbitol) at a dose of 1 g/kg (maximum dose of 30 g) orally, through
nasogastric tube, or as a retention enema. 1 g of resin will bind 1 mEq (mmol) of
potassium. Onset is approximately 1 to 2 hours; may repeat dose after 4 to 6 hours based
upon repeat serum potassium.
Sodium polystyrene sulfonate should not be used in preterm neonates, term neonates with
intestinal hypomotility and/or those at risk for necrotizing enterocolitis, postoperative
patients, or those with bowel obstruction or ileus.
Sorbitol can cause intestinal necrosis and should be avoided. .
Hemodialysis: In children unresponsive to diuretic or cation exchange resin therapy, or
with severe renal dysfunction,Hemodialysis is preferable modality
Consider hydrocortisone 1-2 mg/kg IV if suspicion of adrenal insufficiency
New drug
patiromer is the preferred cation
exchanger. It exchanges calcium ions for
potassium and is approximately 10 times more
potent than sodium polystyrene sulfonate in
potassium removal. However, pediatric data are
not available.
. Sodium zirconium cyclosilicate or ZS-9
is another cation exchange resin that is under
consideration for FDA approval at this time
PEARL:
A. the patient in cardiac arrest with
hyperkalemia should not be pronounced
dead until their potassium level is
normalized
B. If du to digoxin toxicity coexist
calicium C/I,or with precusion slowly.
C.Pitfall: If B-agonists are
given before insulin/glucose they may
cause a transient rise in the serum
potassium level. Always give B-
agonists after insulin/glucose.
Routinely used substances in the treatment approach of
hyperkalemia
substance and dosage Onset Mechanism
Potassium exchange resins (eg,
15‐30 g of calcium resonium
enterally)
>4 h Potassium elimination
Insulin/glucose (eg, 10 IU of
fast‐acting insulin in 25 g of
glucose intravenously)
15‐30 min, maximum effect
at 30‐60 min
Shift of potassium to
intracellular space
Beta‐2 mimetics (eg, 10‐20 mg of
salbutamol per nebulizer or 0.5 mg
of terbutaline
subcutaneously/intravenously)
15‐30 min Shift of potassium to
intracellular space
Loop diuretics (eg, 40‐80 mg of
furosemide intravenously)
5‐30 min Potassium elimination
Calcium (eg, 30 mL of 10%
calcium gluconate or 10 mL of
10% calcium chloride
intravenously)
1‐2 min Myocardial membrane
stabilization
Hyperkalemia new

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Hyperkalemia new

  • 1. Hyperkalemia management Dr.Khalid Hama salih Ass.prof of Pediatrics M.B.Ch. D. C.H F.I.B.M.S.ped University of sulaimany College of medicine Pediatrics department
  • 2. DEFINITION It is defined as a serum potassium concentration greater than 5.5mEq/L The normal serum concentration range for potassium is 3.5-5.0mEq/L  The incidence of hyperkalemia in the pediatric population is unknown, but is considered rare.[7] However, the prevalence of hyperkalemia in extremely low birth weight premature infants can exceed 50%.  The incidence in hospitalized patients ranges from 1% to 10%, and mortality amounts up to 1 per 1000.
  • 3. It can be classified according to severity Mild hyperkalemia-5.5_ 6mEq/L Moderate hyperkalemia-6.1-6.9mEq/L Severe hyperkalemia->7
  • 4. Causes K major mechanisms of true hyperkalemia are Pseudohyperkalemia, usually due to hemolysis of the blood specimen, is the most likely cause of an elevated serum or plasma potassium level in children. Other Leukocytosis or thrombocytosis A.Increased potassium intake B.Tubular unresponsevines to aldosterone C.Redistribution of potassium into extracellular D.Reduced urinary potassium excretion Increased potassium release from cells, most commonly due to (eg, , prolonged seizure, hyperthermia, o exercise), tumor lysis syndrome, massive transfusion, and metabolic acidosis,HYPEROSMOLALITY: (Hypertonic dextrose,Mannitol,iv immunoglobulins ) Medication Eg. NSAID, trimethoprim, heparin, chemotherapy, K- sparing diuretic, ACE inhibitor, beta blockers, succinylcholine, digoxin, mannitol
  • 5. CLINICAL PRESENTATION OF HYPERKALEMIA GENERAL • Related to the effects of excessive k+ on neuromuscular, cardiac & smooth muscle cell function Clinical features • Serum potassium level 5 to 7 mEq/L: Generally asymptomatic • Serum potassium level greater than 7 mEq/L: Muscle weakness, paralysis, and cardiac changes on electrocardiography and arrhythmias. Sudden arrest may occur. SYMPTOM • Frequently asymptomatic however patient may complains of  Dyspnea .palipitation.  Nausea or Vomiting Chest pain
  • 6. Laboratory evaluation •Laboratory tests are based upon probable etiology. All patients with true hyperkalemia should have the following tests obtained: •Blood urea nitrogen (BUN) •Creatinine •Blood glucose •Serum electrolytes •Urinalysis •Urine electrolytes •where adrenal insufficiency is suspected, additional testing includes:Serum cortisol and ACTH (prior to administration of exogenous corticosteroids)
  • 8. Peaked T waves of Hyperkalemia. Note the amplitude of the T exceeds the amplitude of the R. Care of Life in The Fast Lane blog Example of bradycardia with absent or flattened p waves in hyperkalemia
  • 9. Management Management 1.Stop all potassium intake • 4.Remove potassium; 2.Stabilize cardiac membranes with calcium 3.Transe cellular shift calicium :Give only for 1.ECG findings (eg, widening of the QRS complex or loss of P waves, but not peaked T waves alone) or 2.severe arrhythmias thought to be caused by hyperkalemia or in patients with 3. a potassium level ≥7 mEq/L. •For perfusing patients, give calcium gluconate 10% solution 60 mg/kg; given as 0.6 mL/kg diluted in an equal volume of D5W or NS, maximum 2 g (20 mL, 4.5 mmol) per dose IV or IO over 5 minutes. Time to onset of action is immediate. May repeat in 10 minutes as needed for persistent ECG changes or arrhythmias. ¶ •For cardiac arrest, give calcium chloride 10% solution 20 mg/kg given as 0.2 mL/kg, maximum 2 g (20 mL, 14 mmol) per dose; dilute in an equal amount of D5W or NS and give slow IV via central venous access or IO push; repeat in 10 minutes as needed for persistent arrest, ECG changes, or arrhythmias. Δ Insulin and glucose: Onset of action is 10 to 20 minutes. Only give if significant ECG changes or confirmed serum potassium ≥7 mEq/L. Give regular insulin (dose of 0.1 units per kg, maximum dose of 10 units) along with dextrose (glucose) dose of 0.5 g/kg over 30 minutes. The administration of dextrose is based upon the age of the patient as follows:Children younger than 5 years of age: Give 10% dextrose (100 mg/mL) at a dose of 5 mL/kgChildren 5 years of age and older: Give 25% dextrose (250 mg/mL) at a dose of 2 mL/kg. For patients with : a.severe acute symptoms. b.ECG changes, c.arrhythmias, d.impending arrest Larger doses of regular insulin (0.2 units/kg) and dextrose (1 g/kg, 10 mL/kg of 10% dextrose or 4 mL/kg of 25% dextrose) can be administered. Repeat dosing can be given after 30 minutes if needed. The major adverse effect is hypoglycemia, and serum glucose level should be monitored closely and additional dextrose administered as needed. Beta-2 agonist: Onset of action is 20 to 30 minutes. Give nebulized albuterol (salbutamol) with dosing based upon patient weight as follows: Neonates: 0.4 mg in 2 mL of saline Infants and small children <25 kg: 2.5 mg in 2 mL of saline Children between 25 and 50 kg: 5 mg in 2 mL of saline Older children and adolescents >50 kg: 10 mg in 2 to 4 mL of saline (doses up to 20 mg have been used) Inhalation may be repeated after 20 minutes. Inhaled albuterol may also be administered by metered dose inhaler (MDI) as 4 to 8 puffs with spacer. Pitfall: If B-agonists are given before insulin/glucose they may cause a transient rise in the serum potassium level. Always give B-agonists after insulin/glucose. Sodium bicarbonate: Onset of action is 15 minutes. Provides minimal effect on shifting potassium intracellularly and should not be the only therapy used in the management of hyperkalemia, even in acidotic children. Give 1 mEq/kg (1 mmol/kg). Maximum single dose of 50 mEq (50 mmol) which can be provided as 1 mL/kg of 8.4% solution or, for children less than 6 months of age 2 mL/kg of 4.2% solution administered over 10 to 15 minutes. A repeat dose may be given 10 to 15 minutes after last administration. Do not give in the same IV line as calcium because of a risk of precipitation. since the effect of above therapies is transient, treatments to remove potassium are also required: Loop diuretic: Provides only limited short-term effect. Give furosemide 1 mg/kg higher dose may be required with renal insufficiency; fluid losses must be replaced unless the patient is volume expanded. The onset of effect is 1 to 2 hours. May be repeated after 6 hours. Cation exchange resin (sodium polystyrene sulfonate): Give sodium polystyrene sulfonate (without sorbitol) at a dose of 1 g/kg (maximum dose of 30 g) orally, through nasogastric tube, or as a retention enema. 1 g of resin will bind 1 mEq (mmol) of potassium. Onset is approximately 1 to 2 hours; may repeat dose after 4 to 6 hours based upon repeat serum potassium. Sodium polystyrene sulfonate should not be used in preterm neonates, term neonates with intestinal hypomotility and/or those at risk for necrotizing enterocolitis, postoperative patients, or those with bowel obstruction or ileus. Sorbitol can cause intestinal necrosis and should be avoided. . Hemodialysis: In children unresponsive to diuretic or cation exchange resin therapy, or with severe renal dysfunction,Hemodialysis is preferable modality Consider hydrocortisone 1-2 mg/kg IV if suspicion of adrenal insufficiency
  • 10. New drug patiromer is the preferred cation exchanger. It exchanges calcium ions for potassium and is approximately 10 times more potent than sodium polystyrene sulfonate in potassium removal. However, pediatric data are not available. . Sodium zirconium cyclosilicate or ZS-9 is another cation exchange resin that is under consideration for FDA approval at this time
  • 11. PEARL: A. the patient in cardiac arrest with hyperkalemia should not be pronounced dead until their potassium level is normalized B. If du to digoxin toxicity coexist calicium C/I,or with precusion slowly. C.Pitfall: If B-agonists are given before insulin/glucose they may cause a transient rise in the serum potassium level. Always give B- agonists after insulin/glucose.
  • 12. Routinely used substances in the treatment approach of hyperkalemia substance and dosage Onset Mechanism Potassium exchange resins (eg, 15‐30 g of calcium resonium enterally) >4 h Potassium elimination Insulin/glucose (eg, 10 IU of fast‐acting insulin in 25 g of glucose intravenously) 15‐30 min, maximum effect at 30‐60 min Shift of potassium to intracellular space Beta‐2 mimetics (eg, 10‐20 mg of salbutamol per nebulizer or 0.5 mg of terbutaline subcutaneously/intravenously) 15‐30 min Shift of potassium to intracellular space Loop diuretics (eg, 40‐80 mg of furosemide intravenously) 5‐30 min Potassium elimination Calcium (eg, 30 mL of 10% calcium gluconate or 10 mL of 10% calcium chloride intravenously) 1‐2 min Myocardial membrane stabilization

Editor's Notes

  1. Calcium gluconate is a vesicant but can be safely administered through a free-flowing peripheral line in patients with life-threatening hyperkalemia at the dilution shown. Peripheral administration of calcium chloride is not recommended. Sodium bicarbonate should not be administered in the same line. Because the effect of calcium is transient, patients with hyperkalemia also require concomitant or immediate treatments to shift potassium into cells and to remove potassium.