Key facts:
Authors: Stephanie Horne and Andrew Stein
Top Tip: K+ ≥ 6.5 is a medical emergency. Treat it. Recheck it
Key Differential Diagnosis
- Spurious hyperkalaemia (eg if shaken)
Key Investigations
- U+E, LFT, Bone, Glucose, VBG/ABG
- FBC, ESR, CRP
- ECG (any changes, give IV Ca gluconate), CXR
Key Treatment
- Remove underlying cause (esp drugs)
- Rx if K+ ≥ 6.5 mmol/L (or 6-6.4 mmol/L and rising rapidly)
- IV INSULIN 10 (NOT 50) units in 50 mls 50% DEXTROSE over 30 mins; recheck K in 2h; repeat, if necessary, and recheck again
- ± IV 10% CALCIUM GLUCONATE 10 mls
- ± NEB SALBUTAMOL 10 (NOT 5) mg qds
- ± PO SODIUM BICARBONATE 1.2g tds (or IV 1.4% (isotonic) 500 mls over 30 mins or 8.4% 100 mls STAT)
- ± PO CALCIUM RESONIUM 15g qds
Note: only Ca resonium, of these treatments, removes K from the body; the others cause electrolyte shifts; oral NaHCO3 and calcium resonium have no acute effect
Key Management
Decision
- Dialysis (call Renal Unit now)
Background
Common causes are ARF/CRF and drugs, often both. Think about the cause, not just treating it
Introduction
- Hyperkalaemia is one of the most feared of the medical emergencies, but treatment of hyperkalemia is easy
- Hyperkalaemia is a serum K concentration > 5.0 mmol/L, resulting from excess total body K stores or abnormal movement of K out of cells
- Remember K is primarily an intraceullar cation; so the serum level may not reflect what is happening inside the cells, especially the cardiac cells
- The usual causes are impairment of renal excretion (ARF/CRF) or drugs. But it can also occur in metabolic acidosis (as in DKA, initially)
- There are usually no symptoms or signs (except cardiac arrest, when severe!). If clinical manifestations occur, they are generally neuromuscular, resulting in muscle weakness and cardiac toxicity; the latter, if severe, can degenerate to VT/VF (or sometimes) asystole
- Emergency hyperkalemia treatment involves Ca gluconate, insulin/dextrose, loop diuretics and dialysis. If the patient is on dialysis (or has transplant) change of K+ may be more important
Note: ie it is the rate of rise of K that is as/more dangerous than the absolute value. So a patient that goes from 5.0 to 6.0 in 24h is in big trouble; but a well dialysis patient with a pre and post haemodialysis K that is stable at 6.5 and 4.5 may not be
Definition
- Serum potassium >5.0 mmol/L
Epidemiology
- 1-10% of hospital inpatients have hyperkalaemia. This is a large epidemiological study:
[Ref] - 10% of patients on ACEi have raised K+ [Ref]
Severity
- >5.0-5.9 = Mild, but of concern
- >6.0-6.4 = Moderately severe (needs Rx)
- >6.5 = Very severe and immediately life-threatening (do not go home until <6.0)
Causes
'Big three' causes of hyperkalaemia:
- ARF (or ACRF or CRF); some causes of ARF (eg rhabdomyolysis and tumour lysis syndrome) are particlularly likely to cause hyperkalaemia
- Infection
- Drugs (commonly: ACEi, ARB, K+ sparing diuretics (spironolactone, amiloride), K+ containing diuretics; rarely: NSAIDs, calcineurin inhibitors, trimethoprim)
Note: hyperkalaemia often due to a combination of factors; eg ACRF, in a patient on an ACEi, with underlying renovascular disease/CCF, then started on another hyperkalaemic agent (say spironolactone) or becomes dehydrated, due to an infection
Other causes:
- Hypoadrenalism (look for low Na)
- Metabolic acidosis (and causes, eg DKA)
- Massive blood transfusion
- Tissue breakdown (rhabdomyolysis, tumour lysis syndrome ± chemotherapy)
Note: type IV RTA is extremely rare
Symptoms
- Usually nil (underlying disease may cause symptoms - eg SOB in ARF)
- (When severe) generalised muscle weakness
Key question
- "Have there been any changes to your tablets in the last 4-6 weeks?'
Signs
- Usually nil
- Of cause, eg SOB secondary to ARF/CRF
Investigation
If you want to know the K level quickly, do a VBG
Blood
- U+E (if Na low, consider hypoadrenalism), LFT, Bone, Glucose
- VBG (acidosis? lactate?) or ABG, if ?hypoxic
- FBC, CRP, ESR
Other
- CXR
- ECG; often normal; signs can include broad QRS complexes and peaked T waves; reduced/absent P waves or prolonged PR most worrying; abnormalities worsen as K rises:
Note: broad QRS complexes, and peaked T waves
Key investigation
- U+E
Specialist investigation
- 10am cortisol (hypoadrenalism?)
Differential diagnosis
- Spurious hyperkalaemia (if sample shaken)
Treatment
Recheck K 2h after Rx. If you use IV INSULIN, check for hypoglycaemia too. If you are using a second insulin/dextrose, you should be talking to the renal team for a second time
Treatment
(first line)
Remove underlying cause (especially drugs above)
Drugs (If K+ > 6.0)
- IV INSULIN 10 units in 50 mls 50% DEXTROSE over 30 mins (moves K+ back into cells); repeat K in 2h (the effect of insulin/dextrose lasts 4h); and repeat doasge, if necessary (if K still over 6 mcmol/L) and recheck 2h after that; if you have had to give it twice, you should be considering dialysis (ie, involve renal team or ITU); ask the nurses to check BMs regularly, looking out for hypoglycaemia
[Ref] - ± IV 10% CALCIUM GLUCONATE 10 mls (if any ECG changes; stabilises heart)
- ± Nebulised SALBUTAMOL 10 mg qds (NOT 5mg; this does not work); K+ back into cells; transient effect
- ± IV SODIUM BICARBONATE 500 mls 1.4% (isotonic) over 30 mins (if fluid state allows); or 100 mls 8.4% STAT if very unwell, very acidotic, or fluid overloaded; OR PO 1.2g qds, if not. K back into cells. The use of this drug is controversial. But, if patient is severely acidotic, the 'usual' insulin/dextrose and salbutamol will not work; especially if they are in a cardiac arrest state, or very fluid overloaded, giving low volume hypertonic NaHCO3 (ie 100 mls of 8.4%) may be the only way of treating the hyperkalaemia; until dialysis can be organised
- ± PO CALCIUM RESONIUM 15g qds (binds K+ in the bowel
Procedures
- IV
- ECG monitoring (until K+ under 6.0)
Key management decision
- Dialysis/not
Stop
- Drug(s), if cause (eg, ACEi, ARB, K+ sparing diuretics)
Treatment
(second line)
Drugs
- Further round of drug Rx above
- The hypokalaemic effect of loop diuretics can also be useful; ie, if there is any other reason to prescibe one (eg fluid overload), do so
Procedures
- Haemodialysis (if no response to 2 rounds of drug Rx above), or if oligo-anuric; consider haemofiltration on ITU, if hypotensive
- (If unwell) urinary catheter, CVP line, arterial line
Prescribing issues
- Stop salbutamol, when K under control; if nurses will not let you prescribe 10mg of salbutamol, prescribe two 5mg nebulisers 'back-to-back'
Admit?
- If K+ >5.9
Bed plan
- Medical admission ward
- ± Renal, if needs dialysis
- ± Endocrine, if hypoadrenalism
-
± ITU, if unwell, or having arrthymias
Referrals
Medical
- Renal
- ± ITU
Other
- Pharmacist (if think drug cause, but no obvious drug culprit(s))
The Rest
Don't go home till the patient has a K of < 6.0 and falling
Complications
- Cardiac arrest, usually due to tachyarrthymia, especially VT/VF
- Hypoglycaemia (ie consequence of INSULIN Rx)
Prognosis
- Mortality = 15%. 30% with K above 7, 10% if less than 6.5 mmol/L
- Good, if K+ controlled quickly
- Increased risk of death if K+ >6.4, rapidly rising, Creat >135, U>10, PVD, pulmonary disease, digoxin
2° Prevention + Health promotion
- Avoid combinations of ACEi and spironolactone etc
- If on any K+ provoking drug, monitor K+ levels
- Avoid/modify similar chemotherapy regime, if used again
Don't forget
- Mortality = 15%. 30% with K above 7, 10% if less than 6.5 mmol/L
- 1-10% of hospital admissions have hyperkalaemia
- Recheck K 2h after giving insulin/dextrose; repeat dosage if necessary
- Ask nurses to check glucose regularly after insulin/dextrose (?hypoglycaemia)
- Ring GP, if there has been a life-threatening (especially drug-related) episode
- The dose of salbutamol is 10 mg; 5 mg does NOT work
- Oral sodium bicarbonate or calcium resonium have no acute effects
Red flags
- K+ ≥ 6.5 mmol/L; if this case, call your local Renal Unit now
- K+ not < 6.0 after 1st round of medical Rx above; if so, talk to renal team
- Fluid overload
- ECG changes are very serious (give Ca gluconate immediately)
- ARF, with creatinine > 200 mcmol/L
