HYPERKALAEMIA
DEFINITION
A serum potassium concentration greater than 5.5 mmol/L (mEq/L). A
concentration above 6.5 is considered critical.
TOXIC CAUSES
Secondary to excessive potassium intake
High-dose potassium penicillin salts
Large ingestions of potassium salts
Salt substitutes
Slow-release potassium chloride tablets
Rapid or excessive administration of intravenous potassium
Secondary to impaired renal potassium excretion
Angiotensin-converting enzyme (ACE) inhibitors
Non-steroidal anti-inflammatory drugs (NSAIDs)
Potassium-sparing diuretics
Secondary to shift of potassium from cells to serum
Inhibition of Na+/K+ ATPase activity
Digitalis glycosides
Digoxin
Digitoxin
Oleander (Nerium oleander)
Intracellular leakage/transfer
Arginine
Hydrogen fluoride and fluoride salts
Hypertonic solutions
Succinylcholine (in patients with myopathy, recent burns, spinal
cord injury)
Toxic rhabdomyolysis
Toxic haemolysis
Other/Unknown
Alpha-adrenoreceptor agonists
Beta-adrenergic blocking agents
Heparin
Note: Severe hyperkalaemia is rarely a direct complication of acute
poisoning. Most commonly it develops secondary to complications of the
poisoning especially rhabdomyolysis, acute renal failure and metabolic
acidosis.
NON-TOXIC CAUSES
Acidosis
Acute renal failure
Acute tumour lysis syndrome after chemotherapy
Hypoaldosteronism
Primary (Addison's disease)
Secondary
Rapid transfusion of aged blood
Tissue damage (crush injury, burns, infections)
DIFFERENTIAL DIAGNOSIS
Pseudohyperkalaemia
Haemolysis of blood sample
Leukocytosis
Prolonged tight application of tourniquet while drawing blood sample
Thrombocytosis
CLINICAL FEATURES
The important clinical manifestations of hyperkalaemia reflect
membrane depolarisation with decreased conduction velocity and a
faster rate of membrane repolarisation.
The effects of hyperkalaemia on the cardiac conduction system are
initially reflected by electrocardiographic changes which include tall
peaked T waves and ST segment depression. As conduction becomes
further delayed, there is prolongation of the PR interval with
decreased amplitude and disappearance of the P wave and widening QRS
complex with blending of the QRS complex and T wave ("sine wave").
Ventricular tachycardia, ventricular fibrillation or asystole may
ensue.
Neuromuscular features include muscular weakness. A flaccid paralysis
affecting the extremities may occur in severe cases and rarely extends
to involve the trunk and respiratory muscles.
Gastrointestinal effects include abdominal pain (intermittent
intestinal colic), diarrhoea and nausea.
RELEVANT INVESTIGATIONS
Serum potassium
Serum sodium, chloride, and bicarbonate
Renal function tests (urea, creatinine)
ECG (peaked T waves, PR prolongation, QRS widening, bradycardia,
AV block)
Blood glucose
Creatine kinase
Urinalysis (dipstick test for hemoglobinuria/myoglobinuria)
Arterial blood gas analysis
Serum digoxin
TREATMENT
Hyperkalaemia with ECG manifestations and/or a serum potassium
concentration of greater than 6.5 mmol/L is a medical emergency and
requires immediate treatment, starting with establishment of
continuous cardiac monitoring and intravenous access.
Although the underlying causes of hyperkalaemia must be appropriately
managed, life-threatening hyperkalaemia must be urgently treated on
its own merits. Methods available include:
Antagonism of membrane effects of hyperkalaemia
Calcium salts -- either 10% Calcium gluconate or 10%
Calcium chloride (100 mg/mL) is suitable.
Adult dose: 5 to 10 mL (500 to 1 000 mg) IV over 1 to
5 min., may repeat every 5 to 10 minutes up to two times as
required.
Paediatric dose: 0.2 to 0.3 mL/kg (20 to 30 mg/kg) per
dose up to maximum single dose of 5 ml (500 mg) IV over 5 to
10 min., repeated up to four times.
Onset of action: 1 to 5 minutes.
Duration of action: approximately 1 hour.
Notes: (i) Calcium should not be administered to patients
with suspected digoxin toxicity.
(ii) Calcium salts should not be given through the
same line with sodium bicarbonate, as a
precipitate of calcium carbonate may form.
Promotion of shift of potassium to the intracellular space.
Glucose and Insulin
Adult dose: 25 g (250 mL of a 10% solution) dextrose IV
over 30 minutes followed by continued infusion at a slower
rate. Five units of regular insulin per 25 g glucose are
added to the infusion. Alternatively, 50 mL of a 50%
dextrose solution with 5 units of regular insulin may be
administered IV over 5 minutes.
Paediatric dose: 0.5 to 1 g/kg of dextrose followed by
1 unit of regular insulin IV for every 5 g of glucose
infused. This dose may be repeated every 10 to 30 min.
Onset of action: 30 to 60 minutes.
Duration of action: 4 to 6 hours or while infusion
continues.
Sodium bicarbonate -- 8.4% Sodium bicarbonate solution (1 mL =
1 mmol = 1 mEq)
Adult dose: 50 mL IV over 5 minutes, repeated at 20 to 30
minute intervals.
Paediatric dose: 1 to 2 mL/kg/dose IV every 2 to 4 hours
or as required by pH.
Onset of action: 10 to 15 minutes.
Duration of action: 1 to 2 hours.
Removal of Potassium from the body.
Cation-exchange resins. These orally or rectally adminstered
agents exchange K+ for Na+ or Ca++. Suitable agents
include Sodium Polystyrene Sulfonate (Kayexalate(R) , Resonium
ţA(R)) and Calcium Polystyrene Sulfonate (Calcium Resonium(R),
Resonium Calcium(R)).
Adult dose: Oral: 60 mL of suspension (15 g of resin) 1 to
4 times per day as needed.
Rectal: 30 to 50 g of resin as a retention enema following a
cleansing enema. Dilute with sorbitol or 20% dextrose in
water. Enema must be retained for 30 to 45 minutes.
Paediatric dose: Approximately 1 g of the resin/kg/dose
given orally every 6 hours or rectally every 2 to 6 hours.
Note: Do not use Calcium Polystyrene Sulfonate in digoxin
poisoning.
Dialysis. Peritoneal and haemodialysis are effective methods
for removing potassium. Haemodialysis is indicated in patients
who cannot tolerate fluids or have kidney dysfunction.
Intravenous diuretics (thiazides, loop diuretics). The dose
required depends on renal function.
Specific antidotal measures
Digoxin specific antibody fragments are effective in lowering
the potassium in patients with acute cardiac glycoside
intoxication.
CLINICAL COURSE AND MONITORING
If hyperkalaemia occurs in intoxicated patients as a secondary
complication (e.g. rhabdomyolysis, acute renal failure and/or systemic
acidosis), the clinical course is usually determined by the nature and
severity of the underlying poisoning and its complications.
The treatments described above are most likely to be required in cases
of poisoning which involve an increase in the total body potassium
load, such as the ingestion of a large amount of a potassium salt. In
poisoning by digoxin or other cardiac glycosides, normal potassium
homeostasis is usually restored once Na+/K+ ATPase activity is
reactivated by appropriate antidote administration.
Continuous monitoring of cardiac rhythm and ECG parameters together
with careful monitoring of serum potassium and other electrolyte
concentrations, acid-base status, blood glucose, and renal function is
indicated until hyperkalaemia and the underlying cause are controlled.
LONG-TERM COMPLICATIONS
Brain or other organ injury may occur as a result of cardiac arrest
secondary to hyperkalaemia.
AUTHOR(S)/REVIEWERS
Author: Dr Barbara Groszek
Department of Clinical Toxicology, Jagiellonian
University
31-826 Kraków, Os. Zlota Jesien 1
Poland
Reviewers: Birmingham 3/99: B Groszek, H Kupferschmidt,
N Langford, K Olson, J Pronczuk.