Severe Hyperkalaemia

Introduction

When Serum potassium > 5.5 but >7.0 mmol/L is a medical emergency

Etiology

1. Acute kidney injury/ Acute renal failure (severe)
2. Chronic Kidney Disease/Chronic renal failure (advanced)
3. Drugs:

ACE inhibitors/ACE blockers

Amiloride

Triamterene

Spironolactone/eplerenone

NSAIDs

Ciclosporin treatment

Heparin treatment

4. Redistribution of cells

Beta blockers

Acidosis

Hyperkalaemic periodic paralysis – (an autosomal dominant condition) precipitated by exercise.

Severe hyperglycaemia

5. ↑ K intake or load

Diet,

IV therapy

6. Adrenocortical failure (Addison’s disease)

Patho-physiology

Hyperkalaemia causes depolarization of cell membranes, leading to decreased cardiac excitability, hypotension, bradycardia and eventual asystole.

Clinical assessment

can present with progressive muscular weakness
sometimes there are no symptoms until asystolic cardiac arrest occurs

Investigations

• ECG- Though this is a poor predictor of cardiac toxicity.

For Underlying aetiology-

• Creatinine
• Electrolytes and bicarbonate,

In  Adrenocortical failure (Addison’s disease)- Characteristically low Na+ (although this can occur in many causes of hyperkalaemia ).
(Addison’s disease should be excluded unless there is an obvious alternative diagnosis).

Management of severe hyperkalaemia

Treatment for severe hyperkalaemia requires both urgent measures for life saving and maintenance therapy to keep normo kalaemia.
For significant hyperkalemia (plasma K+ concentration 6.5–7 mM) should be aggressively managed-

• Continuous cardiac monitoring

Immediate

1. Continuous cardiac monitoring

Membrane stabilizer.

2. 10 mL of 10% calcium gluconate iv over 3-5 min (can be repeated after 15 min if there is no change in ECG findings)

or

calcium chloride 5%, 5–30 mL intravenouslyC

Adv-

The effect of the infusion starts in 1–3 min and lasts 30–60 min

Drive K+ into cells

3. Insulin (Short Acting) 10 units + 50 mL of 50% glucose iv. over 10– 15 min (25 g of glucose total);

Adv-

the effect begins in 10–20 min, peaks at 30–60 min

Caution-

4. Hypoglycemia is common with insulin plus glucose, hence, this should be followed by an infusion of 10% dextrose at 50 to 75 mL/h, with Regular checks of blood glucose and plasma K+.

and/or

5. Inhaled β₂ agonist,
1. Albuterol- (most commonly)H,C 10–20 mg of nebulized albuterol in 4 mL of normal saline, inhaled over 10 min.

Or,

2. salbutamol 5 mg in 100 mL of 5% glucose over 15 min (rarely used)^K

Adv-

the effect starts at about 30 min, reaches its peak at about 90 min, and lasts 2–6 h

Caution-

• Common side effect are Hyperglycemia is a along with tachycardia
• should be used with Caution in known cardiac disease.
5. NaHCO3 (1.26%) 44–88 mEq (1–2 ampules) intravenously

Caution:

• Intravenous bicarbonate has no role in the routine treatment of hyperkalemia.
• It should be reserved for patients with hyperkalemia and concomitant metabolic severe acidosis  (pH <6.9)
• Sodium bicarbonate may not be effective in end-stage renal disease patients.

Late

Remove K⁺ from body

7. Polystyrene sulphonate resins:

Oral: 15–30 g in 20% sorbitol (50–100 mL) up to three times daily^C

Rectal: 50 g in 20% sorbitol^C

Alternatively-

15 g orally up to three times daily with laxatives 30 g rectally followed by 9 hrs later by an enema^P.

Adv-

Duration of Treatment is 1–3 hours.

Caution:

Resins with sorbitol may cause bowel necrosis and intestinal perforation^C.

8. i.v. furosemide and normal saline 40–160 mg intravenously or orally (If adequate residual renal function)^D

Caution:

Diuretics may not be effective in patients with acute and chronic kidney diseases^C.

9. Haemodialysis or peritoneal dialysis if the above fails.