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K
Disorders
Dr. Mohammed Kamal
NephrologySpecialist
MansouraInternational Hospital
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 as plasma concentration of K+ < 3.5 mEq/L
Mild Hypokalemia : 3.0 – 3.5 mEq/L :
asymptomatic
Hypokalemia 2.5 to 3.0 mEq/L : Moderate, may be
symptomatic
Hypokalemia < 2.5 mEq/L : Severe, may be
symptomatic
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)
Due to
Decreased net intake :Uncommon
Shift into cells
Increased net loss
Cause is usually apparent on HISTORY and
physical examination.
DIAGNOSIS –
ETIOLOGY
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
MANAGEME
NT
• In Severe Hypokalemia(Potassium <2) or
symptomatic patients IV Correction
required,
ECG monitoring
Frequent testing
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
Patients with Asthma , Heart disease and
patients on medications that cause polyuria or
loss of K in urine
Patients who have rhythm
abnormalities( Bradycardia,hypotension,low
volume pulse(
HYPERKALEMIA
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 potassium-
sparing 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 hrs
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
HYPOKALEMIA---TAKE HOME
MESSAGE
Anticipate Hypokalemia in patients with
diarrhea,patients 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-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.
Hypokalemiaandhyperkalemiaindorepedicon2014final 140112051537-phpapp01(1)

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Hypokalemiaandhyperkalemiaindorepedicon2014final 140112051537-phpapp01(1)

  • 2. 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
  • 3. HOW INTRACELLULAR K+ CONTENT IS MAINTAINED
  • 4. HYPOKALEMIA Defined as plasma concentration of K+ < 3.5 mEq/L Mild Hypokalemia : 3.0 – 3.5 mEq/L : asymptomatic Hypokalemia 2.5 to 3.0 mEq/L : Moderate, may be symptomatic Hypokalemia < 2.5 mEq/L : Severe, may be symptomatic
  • 5. 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
  • 7. 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)
  • 8. Due to Decreased net intake :Uncommon Shift into cells Increased net loss Cause is usually apparent on HISTORY and physical examination. DIAGNOSIS – ETIOLOGY
  • 9. 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)
  • 10. 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(
  • 11.
  • 12.
  • 13. 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
  • 14. 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
  • 15. MANAGEMENT Reduction of potassium losses Replenishment of potassium stores
  • 16. 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
  • 17. REPLENISHMENT OF POTASSIUM STORES Patients who have mild or moderate hypokalemia ( 2.5-3.5 mEq/L) ;asymptomatic patients: ORAL THERAPY PREFERRED
  • 18. MANAGEME NT • In Severe Hypokalemia(Potassium <2) or symptomatic patients IV Correction required, ECG monitoring Frequent testing
  • 19. 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
  • 20. REVISION—WHICH PATIENTS CAN HAVE HYPOKALEMIA Neuromuscular weakness (AFP) esp.if recurrent, unable to wean off ventilator. Unexplained abdominal distension,constipation Patients with Asthma , Heart disease and patients on medications that cause polyuria or loss of K in urine Patients who have rhythm abnormalities( Bradycardia,hypotension,low volume pulse(
  • 21.
  • 22.
  • 24. HYPERKALEMIA K+ above 5.5 mEq/L, Premature infants /young children upto 6.5 mEq/L normal.
  • 25. FACTORS INCREASING K+ Alpha-adrenergic agents(Impairs cellular K+ uptake) Acidosis (Impairs cellular K+uptake) Cell damage (Intracellular K+release) Hypoaldosteronism
  • 26. 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).
  • 27. IS THIS LAB REPORT CORRECT? Fictitious Hyperkalemia : hemolysis, "milking" of extremities , thrombocytosis or leucocytosis.
  • 29. 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 potassium- sparing diuretics).
  • 30. INCREASED K+ INTAKE Intravenous or oral potassium supplementation. Packed RBCs (PRBCs)transfusion
  • 31. 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.
  • 32. 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
  • 33. ECG CHANGES Tall Peaked T waves (K 6.5) Prolonged PR, Flat or absent P waves(K 7.5)
  • 34. ECG CHANGES Widened QRS (>0.12 Sec) , Sine wave pattern(S and T waves merging) (K 8.5)
  • 36. MANAGEMENT Immediately discontinue any IV potassium containing fluid/any drugs that may cause hyperkalemia.
  • 37.
  • 38. 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
  • 39.
  • 40. 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)
  • 41. 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.)
  • 42.
  • 43. 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 hrs
  • 44. 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
  • 45. C BIG K DROP C : Calcium Gluconate B: Bicarbonate I,G : Insulin and Glucose K: Kayexelate D: Diuretics and Dialysis
  • 46.
  • 47. HYPOKALEMIA---TAKE HOME MESSAGE Anticipate Hypokalemia in patients with diarrhea,patients 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
  • 48. 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.