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Hyperkalaemia
• Commonly encountered in clinical practice.
• Changes in plasma K mean that “excitable”
cells, such as nerve and muscle, may respond
differently to stimuli.
• Heart is nerve and muscles.
Serum potassium and K balance
• 3.5-5.3 mmol/L.
• Potassium losses (through the kidneys) usually
mirror intake.
• 98 % of K is inside
cells.
Hyperkalaemia
• If severe (> 7 mmol/L) is immediately lifethreatening.
• Cardiac arrest may be the first manifestation.
ECG changes seen in hyperkalaemia.
• Other symptoms
- Muscle weakness
- Paraesthesiae.
Hyperkalaemia
•
-
Could be due to:
Decreased excretion.
Redistribution out of cells.
Increase intake.
Hyperkalaemia –
1- Decreased excretion
• In Practice, all patients with hyperkalaemia
will have a reduced glomerular filtration rate
(GFR).
• Renal failure:
- GFR is low > Kidneys may not be able to
excrete K.
- Exacerbated by metabolic acidosis (increase
organic ions.
Hyperkalaemia –
Decreased excretion
• Hypoaldosteronism:
- Aldosterone stimulates the reabsorption of Na in
the renal tubules at the expense of K and H ions.
- Deficiency, antagonism or resistance results in Na
loss, causing decreased GFR, retention of K and H
ions.
- Most often by using hypertension drugs.
- Less common adrenal insufficiency is responsible.
Hyperkalaemia –
2- Redistribution out of cells
• Potassium release from damaged cells:
- Concentration of K inside cells (140 mmol/L)
- Rhabdomyolysis (skeletal muscle is broken
down).
- Extensive trauma.
- Rarely, tumour lysis syndrome (malignant cells
beak down).
- Haemolysis.
Hyperkalaemia –
Redistribution out of cells
• Metabolic acidosis:
- Reciprocal relationship between K and H ions.
to maintain electrochemical neutrality.
Hyperkalaemia – Redistribution out of
cells
•
•
-
Insulin deficiency:
Insulin stimulates cellular uptake of K.
Important in treatment of hyperkalaemia.
Deficiency and resistance.
Feature of diabetes ketoacidosis.
Hyperkalaemic periodic paralysis:
Rare familial disorder with autosomal dominant
inheritance.
- Typical recurrent attacks of muscle weakness or
paralysis.
Hyperkalaemia – Redistribution out of
cells
• Pseudohyperkalaemia:
- Increase concentration of K due to movement
out of cells during and after venesection.
- Commonest causes:
1- delay in centrifugation separating
plasma/serum from the cells/clot, especially it
the specimen is chilled (primary care).
2- in-vitro haemolysis.
3- increase in platelet and/or white cell count.
Hyperkalaemia –
3- increase intake
• Dangerous particularly in patients with
impaired renal function.
• Oral drugs as potassium salt.
• Intravenously (more than 20 mmol/hour is not
recommended).
• Blood transfusion (less than 5 days old) and/or
by washing units prior to transfusion.
Treatment
• Calcium: counteract the effect of
hyperkalaemia in resting membrane potential
of cells.
• Insulin and glucose: to promote the uptake of
K by muscle tissues.
• Low GFR should be assessed. (if not dialysis is
needed).
Hypokalaemia –
1- reduced intake
• Rare.
• Since K is present in meat, fruit and some
vegetables, marked K restriction is difficult to
maintain.
• Hypocaloric diet !
Hypokalaemia –
2 - redistribution into cells
• Metabolic alkalosis: Reciprocal relationship
between K and hydrogen ions, as the
concentration of hydrogen ions decreases, so
K ions move inside cells.
Hypokalaemia –
redistribution into cells
• Treatment with insulin: risk when treatment of
diabetic ketoacidosis.
• Refeeding: “refeeding syndrome” first described
in prisons of wars. It occurs when previously
malnourished patients are fed with high carbs
results in rapid fall in phosphate, Mg, and K.
Mediated by insulin as it moves glucose into cells.
- Anorexia nervosa
- Cancer
- Alcoholism
- Postoperative patients.
Hypokalaemia –
redistribution into cells
• Treatment of anemia: uptake of K by new
blood cells.
• Hypokalaemia periodic paralysis: can be
inherited (autosomal dominant trait).
Hypokalaemia –
3- increase losses
• Gastrointestinal: Cholera (massive fluid loss from
gut)
• Urinary:
- Diuretics: drugs (thiazide), hyperaldoseronism.
- Mineralocorticoids excess
- Hypomagnesaemia: impaired renal tubular
absorption.
- Tubulopathie: chemotherapy (platinum
containing drugs)
Hypokalaemia - treatment
• Potassium salts are unpleasant to take orally
and are usually given prophylacti- cally in an
enteric coating.
• Severe potassium depletion often has to be
treated by intravenous potassium. Intravenous
potassium should not be given faster than 20
mmol/hour except in extreme cases and
under ECG monitoring.
Determination of sodium
• Specimen: serum, plasma, urine (24 hours).
• Suitable anticoagulants: lithium heparin,
ammonium heparin, lithium oxalate.
• Hemolysis does not cause significant change in
serum or plasma values, except in marked
hemolysis levels.
Reference range
Serum, plamsa
133-146 mmol/L
Urine 24 hours
40-220 mmol/L (diet)
CSF
133-150 mmol/L
Chemical method
• Photometric determination of serum sodium
Mg- Uranylacetate method
• Principle: Sodium is precipitated with MgUranyl acetate; the uranyl ions remaining in
suspension form a yellow-brown complex with
thioglycolic acid. The difference between
reagent blank (without precipitation of
sodium) and analysis is proportional to the
sodium concentration.
Ion-selective electrode (ISE)
• Is a sensor that
converts the activity
of specific ion
dissolved in a
solution into an
electric potential,
which can be
measured by a
voltmeter of pH
meter.
Vitros
Determination of potassium
• What are the causes of artifacual
hyperkalaemia?
- Sample hemolysis
- Thrombocytosis
- Prolonged tourniquet use of excessive fist
clenching.
- Determination by ISE
Reference range
Serum,
3.5-5.1 mmol/L
Plamsa
Male: 3.5 – 4.5 mmol/L
Female: 3.4 – 4.4 mmol/L
Urine 24 hours
25-125 mmol/L