EM guidemap - Hyperkalemia

Click on any of the headings or subheadings to rapidly navigate to the relevant section of the guidemap

Introduction

History of the present illness

Risk factors

Examination

Diagnostic testing

Medical decision-making and treatment Appendix
Introduction

- this guidemap is mainly focused on the ED management of life-threatening hyperkalemia

- to determine the likely cause of the hyperkalemia (if the etiology is not clinically evident) => use the algorithm for the diagnosis of hyperkalemia in conjunction with the table listing causes of hyperkalmia

History of the present illness

- neurological symptoms

- cardiovascular symptoms - hyperkalemia is frequently discovered as an incidental or unexpected finding in a patient with no specific symptoms to suggest the diagnosis

Risk factors

- renal failure

- hypoaldosteronism - tubular unresponsiveness to aldosterone/drugs affecting tubular sodium-potasium exchange - obstructive uropathy

- redistribution of potassium

- pseudohyperkalemia (* Pseudohyperkalemia - first exclude hemolysis by inspecting a centrifuged blood specimen's supernatant fluid => pseudohyperkalemia is present when the plasma potassium [heparinised tube] is more than than 0.3meq/L greater than the serum potassium)

Examination

- first check the patient's ABC’s with a special emphasis on the evaluation of any respiratory depression

Diagnostic testing

ECG

There is no definite correlation between any ECG changes and the serum potassium - the relationship depends on individual patient sensitivity and the rapidity of development of the hyperkalemia

(* ECG signs may be absent if the onset of hyperkalemia is slow - as seen in chronic renal failure - even though the serum potassium is in the range of  7 - 7.5meq/L; by contrast, acute hyperkalemia can produce ECG signs at much lower serum potassium levels)

- tall peaked T waves with a narrow base (called "tenting") or even more exaggerated "thorn-like" peaked T waves, an increased PR interval, and a slightly prolonged QRS duration suggest a serum potassium > 6 - 7 meq/L

- P wave flattening => absent P waves and/or marked QRS widening suggest a serum potassium > 7 - 8 meq/L

- fusion of the widened QRS complex and a tall T wave forming a sine wave suggests a serum potassium > 8 - 9 meq/L

- certain ECG changes may mimic an AMI

- other typical ECG patterns include the "dumping" pattern and the "z-fold" pattern

- varying degrees of heart block and ventricular tachyarrhythmias

- the progression from benign to malignant arrhythmias can be rapid and unpredictable

- any diagnostic ECG change represents an emergency requiring aggressive therapy

(* see the appendix for samples of ECG changes in hyperkalemia)

Lab tests

- serum electrolytes, calcium, serum digoxin, BUN and creatinine, glucose +/- ABG’s

(* consider Addison's disease in a hyperkalemic patient who has associated hyponatremia and postural hypotension => diagnosed by a low serum cortisol and lack of response to a synthetic ACTH injection)

- plasma renin and plasma aldosterone levels prn in patients with a history of diabetes mellitus, or if there is a suggestion of some type of tubulo-interstitial renal disease, or when the etiology is not readily apparent

Medical decision-making and treatment

- continuous cardiac monitoring is mandatory if the patient has severe hyperkalemia (serum potassium > 6.5 MEq/L) or cardiac arrhythmias

- a patient with mild-moderate hyperkalemia (serum potassium < 6.0 meq/L) can be treated with dietary restriction + discontinuation of any potassium sparing diuretic +/- a potassium-binding resin eg. sodium polystyrene sulfonate (Kayexalate) = 15 - 30 g qd/qid => the patient can be discharged and followed-up in 48 - 72 hours

- a patient with moderate hyperkalemia (serum potassium 6.0 - 6.5 mEq/L) should probably be admitted to hospital for supervised lowering of the serum potassium with a potassium-binding resin

- treat hyperkalemia more emergently if the serum potassium is > 6.5 meq/L or if there are any ECG changes suggestive of hyperkalemia => use sodium polystyrene sulfonate as first line therapy +/- insulin/glucose +/- calcium gluconate

The following drug order sequence is recommended for life-threatening hyperkalemia (absent P waves + widened QRS complex, and/or serum potassium > 8 meq/L, and/or significant cardiovascular symptoms or arrhythmias, and/or severe neuromuscular symptoms)

1) Calcium gluconate

- there is no "correct" dose

- 10 ml of 10% calcium gluconate solution over 10 minutes IV (rule of "tens") is a common approach

- calcium chloride can be used at 1/3 the dose of calcium gluconate

(* calcium should preferably be administered in large veins because it is sclerosing)

- works in 1 - 3 minutes and lasts 30 - 60 minutes

- repeat dose in 5 - 10 minutes if no ECG change/improvement

- initial dose can be given in 1 - 3 minutes for life-threatening arrhythmias or sine wave ECG changes, and repeated every 2 - 5 minutes prn

- short-half life requires repeat dosing every 20 minutes prn

(* calcium only antagonises potassium's deleterious electrical effect on the myocardium and it does not decrease the serum level of potassium - it is used temporarily until the serum potasium can be decreased by insulin + glucose administration)

- pediatric dose = 75 - 100 mg/kg IV (0.75 - 1.0 cc/Kg to maximum of 10 cc)

- special warnings:-

2) Insulin + Glucose

- insulin + glucose is used to drive potassium into the cells

- 10 units insulin by rapid IV bolus + 50ml of 50% dextrose IV over 20 - 30 minutes; or the insulin can be mixed with 100 ml of 20% dextrose solution and administered IV over 20 - 30 minutes

- glucose should not be given to diabetics without first giving insulin - because insulin is needed to move potassium into the cells; also avoid giving 50% glucose by rapid IV bolus injection

(* rapid bolus injection of concentrated glucose => hypertonicity-induced potasium redistribution => temporary increased serum potassium before the insulin takes effect)

- pediatric dose = 0.1 unit/kg of insulin + 25% glucose (0.5 mg/kg - 2ml/kg of 25% concentration)

- onset occurs within 15 - 60 minutes and effect lasts 4 - 6 hours

- follow-up 10% glucose solution at 50 - 100cc/hour is rarely needed - only if the patient develops hypoglycemia secondary to the IV insulin bolus

(* IV glucose is not indicated when the serum glucose is greater than 250mg/ml => check the serum glucose frequently to detect delayed-onset hypoglycemia)

3) Albuterol by nebuliser

- 10 - 20mg in 4 ml saline over 10 - 20 minutes (large doses required)

(* may need to be given undiluted over 5 - 10 minutes in a patient with life-threatening hyperkalemia)

- immediate onset and maximum effect in 90 - 120 minutes

- decreases serum potassium by about 0.5 - 1.0 meq/L

- pediatric dose = same as the adult dose

(* small risk of tachyarrhythmias => stop if PVC's develop)

4) Bicarbonate

- only indicated when the patient is significantly acidotic (serum bicarb < 5 - 10)

- beneficial effect is small and inconsistent

- useful if the patient is also sodium/volume depleted  => use 3 amps of bicarb in 1L of 5DW at desired rehydration rate

- more rapid administration of bicarbonate (1 amp over 10 - 15 minutes) should be reserved for severely acidotic patients with sine wave QRS changes

- pediatric dose = 0.5 - 1.0 meq/kg

(* sodium load worsens hypertension and may induce CHF in vulnerable patients)

5) Kayexalate - sodium polystyrene sulfonate

- defer if the patient is going to be dialysed within 2 hours to avoid a "colonic laundry"

- po route preferred if possible (greater degree of cation exchange)

- 15 - 50g in 100cc of 70% sorbitol po (or use commercial preperation)

- onset within 1 - 2 hours and lasts 4 - 6 hours

- dose can be repeated q 4 hourly, up to 5x doses/day prn

- use a retention enema if po administration is not preferable/possible

- use a retention enema of 50 - 100g kayexalate + 50cc of 70% sorbitol + 150cc tap water, or suspend the powder in 10% dextrose solution, or use 120 - 180cc of the commercially available suspension

- the retention enema is administered through a 24 - 28g rectal tube placed 20cm into rectum after any necessary pre-cleansing enema, followed by a saline flush of 50cc

- a retention enema must be retained for at least 30 - 60 minutes, preferably 1 - 2 hours

(* po administration may produce nausea and vomiting; retention enema with sorbitol - risk of colonic perforation in post-op renal transplant patients and therefore contra-indicated; risk of volume overload from sodium load whether given po or by retention enema)

- pediatric dose = 0.5 - 1g/kg po (maximum of 50g) or 1 - 2g/kg rectally (mixed in 70% sorbitol solution)

6) Lasix

- 40 - 80 mg of lasix IV to all patients who can produce urine

- pediatric dose = 1 mg/kg IV

7) Dialysis

- primary therapy when renal function is absent

- prompt dialysis may also be required in patients with ARF + associated rhabdomyolysis (large potasssium load)

- also used for intractable hyperkalemia unresponsive to conservative pharmacological measures

8) Treat any underlying cause of the hyperkalemia

- treatment is disease-specific

Appendix

ECG changes in hyperkalemia

Causes of hyperkalemia
 Pseudohyperkalemia
  • tight tourniquets and/or fist clenching 
  • small needle and/or venous sampling in a high vacuum tube
  • over-vigorous centrifugation of the blood specimen and/or laboratory error 
  • red cell hemolysis
  • thrombocytosis
  • marked leucocytosis
  • abnormal red cell membrane and potassium leakage 
 Excess potassium intake
  • transfusion of old blood
  • IV potassium administration
  • KCl-containing salt substitutes
  • Drugs containing potassium - IV penicillin, potassium citrate
  • Unusual po sources - geophagia (clay soil), cautopyreiphagia (burnt match heads), black molasses
 Redistributional or transcellular shifts
  • cellular damage - burns, crush injury
  • IV hemolysis
  • tumor lysis
  • rhabdomyolysis
  • acidemia
  • hypertonicity - mannitol, hyperglycemia
  • medications - digoxin, somatostatin, succinylcholine, beta blockers
  • severe physical exertion
  • prematurity (first 72 hours of life)
  • fasting in a dialysis patient
  • toxins - palytoxin, tetrodotoxin, hydrofluouric acid, cocaine 
  • familial hyperkalemic periodic paralysis
 Adrenal-renal
  • lack of renin substrate - very advanced liver failure
  • hyporeninemia - diabetic nephropathy, interstitial nephritis, type IV RTA, drugs (NSIAD's, beta-blockers, heparin, cyclosporine)
  • decreased aldosterone synthesis - congenital adrenal disease (21 hydroxylase enzyme deficiency and other specific synthetic defects) or acquired adrenal disease (Addison's disease, TB of the adrenals) 
  • absence or blockade of the aldosterone receptors - pseudohypoaldosteronemia type I, drugs (spironolactone,amiloride, triamterine, cyclosporine, trimethoprim, pentamidine)
 Acute renal failure

 Chronic renal failure

 Urinary tract obstruction

 Tubular defects in potassium secretion

  • interstitial nephritis
  • SLE
  • sickle cell disease
  • diabetic nephropathy
  • amyloidosis
  • renal allograft
  • drugs - sulfas, penicillin, rifampin, NSIAD's

Algorithm for the diagnosis of hyperkalemia

Disclaimer: My EM guidemaps reflect my personal approach to problem-solving/managing clinical cases in an ED setting and they should not be regarded as the standard of care. They merely represent the personal opinions of the author and they should only be used in clinical practice if the reader-user has substantial reason to believe that the clinical advice contained in the guidemaps is valid and accurate. The guidemaps are not meant to be "authoritative" and the reader-user should consult standard medical textbooks and expert opinion articles/guidelines for more authoritative advice. The reader-user should particularly confirm all drug doses, their indications and contra-indications, prior to their use.