Episode 189: Hyperkalemia 2.0

We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma)

Hosts:

Brian Gilberti, MD

Jonathan Kobles, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3



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Tags: Renal Colic

Show Notes

Introduction

Background

Physiology:

Normal range and the significance of deviations (>5.5 mEq/L)

Epidemiology:

Prevalence of hyperkalemia in the ER
ESRD missed HD → ECG, monitor

Causes / Risk Factors

Causes

Kidney Dysfunction, Medications,  Cellular Destruction,  Endocrine Causes, Pseudohyperkalemia

High-Risk Medications:

Antibiotics: Bactrim, antifungals

Calcineurin inhibitors

Beta-blockers

We revisit the topic of Hyperkelamia to update our prior episode from 2015 (pre-Lokelma)

Hosts:

Brian Gilberti, MD

Jonathan Kobles, MD

https://media.blubrry.com/coreem/content.blubrry.com/coreem/Hyperkalemia.mp3



Download


2 Comments





Tags: Renal Colic

Show Notes

Introduction

Background

Physiology:

Normal range and the significance of deviations (>5.5 mEq/L)

Epidemiology:

Prevalence of hyperkalemia in the ER
ESRD missed HD → ECG, monitor

Causes / Risk Factors

Causes

Kidney Dysfunction, Medications,  Cellular Destruction,  Endocrine Causes, Pseudohyperkalemia

High-Risk Medications:

Antibiotics: Bactrim, antifungals

Calcineurin inhibitors

Beta-blockers

ACE/ARB

K+ Sparing diuretics

NSAIDs

Digoxin

SUX – high risks in neuromuscular disease

Lab errors, hemolysis in samples

VBG vs Chem accuracy 
When to repeat a hemolyzed sample 
2023 study: Of the 145 children with hemolyzed hyperkalemia, 142 (97.9%) had a normal repeat potassium level. Three children (2.1%) had true hyperkalemia: one had known chronic renal failure and was referred to the ED due to concern for electrolyte abnormalities; the other 2 patients had diabetic ketoacidosis (DKA).

Clinical Presentation / eval 

Symptomatic vs. Asymptomatic:

“First symptom of hyperkalemia is death” 
If severe, ascending muscle weakness → paralysis 

Point at which patients experience symptoms depends on chronicity

>7 mEq/L if chronic and can be lower if acute

Hyperkalemia can be a cause of non-specific GI symptoms

EKG Changes:

ECG findings may be the first marker the ER doc gets that something is wrong
Typical changes: 

Peaked T-waves, shortened QT
Lengthening of PR interval and QRS duration 
Bradycardia / Junctional rhythm

Hyperkalemia can produce bradycardia without other ECG findings

Ones associated with VT/VF/code, death in one study: QRS widening (RR = 4.74), Junctional Rhythm (RR = 7.46), HR <50 (RR = 12.29) while no adverse outcomes with just peaked T waves or PR prolongation (Durfey, 2017)

Don’t be fooled by a normal ECG, may be normal, but it’s also on case report level to have K > 9 and a normal ECG

Series of 127 patient (K 6-9.3), no serious arrhythmia noted, only 46% had ECG changes, (Acker, 1998)

ECG changes are not linear, there is no exact association between K+ levels and ECG changes
ECG changes may be hidden and subtle in patients with underlying inter-ventricular conduction delay (BBBs)

Be suspicious of the patient with LBBB > 160 ms or RBBB > 140 ms

BRASH Syndrome

Synergism between hyperkalemia, renal failure/injury and AV nodal blocking agents -> may produce ECG changes out of proportion to serum potassium levels. 

Labs

Chem, VBG, +/- CK if you think muscle breakdown is at play (Tintinalli talks about looking at urine K, but this is not most people’s practice)
Consider evaluation for adrenal insufficiency
Waiting for labs may not be an option

Renal dysfunction + consistent ECG findings → prompt treatment before chem results
Realistically 2 hours to get back chemistry in most settings ≈ eternity

Management in the ER

Discontinue/hold any nephrotoxins or medications in suspected medication-induced hyperkalemia

A. Acute Management Strategies:

Cardiac protection with calcium

1g over 5-10 mins

Lasts 30-60 mins, may have to redose 
Dose considerations if on digoxin 
AEs: Calciphylaxis and hypercalcemia

Fast pushes can result in hypotension, arrhythmia

Calcium chloride vs calcium gluconate
Caution in patients taking Digoxin

IVF choice – NS vs LR

Caution/Avoid fluid in patients with ESRD/CHF or signs of VOL

Shifting potassium: 

insulin/glucose

5 units vs 10 units 

5 similar effect, less hypoglycemic episodes (LaRue 2017)
If doing 10 units, start D10W at 50-75 cc/h after amp of d50 but be mindful that anuric patient who missed HD may not have much room for volume 

Decrease but about 0.5-1.2 mEq/L
Effect starts 10-20 mins after administration and can last 4-6 hours

Albuterol

10-20 mg over 10 mins (NB: higher dose than for asthma)
Peak effect at 90 mins
Decreases by 0.5 – 1.0 mEq/L alone

With insulin, ~1.2 mEq/L, additive effect 

Bicarbonate

Controversy. Useless in hyperkalemic, nonacidotic patient. Useful as drip but takes hours to work, again, volume in anuric patient an issue 

May be most useful in patients with renal failure and hyperkalemia 2/2 volume loss

Hypertonic Bicarb is ineffective – More potassium is pulled out of cells due to osmotic shift.

Removal: 

Lokelma (Sodium Zirconium cyclosilicate)

Luckily residents have never had to use Kayexalate
Can start working in 1-2 hours of administration 
0.37 mEq/L reduction at 4 hours after 10 g
Not a magic bullet in patients who need dialysis

Diuretics

No studies that demonstrate effectiveness in this ED setting

May be effective in patients with normal renal function

If patient not anuric, may be worth using, can give 40 mg, but again, should not be the only attempted method of removing K
Nephron BOMB

Loop Diuretic (160-250 mg IV Lasix or 4-5 mg IV Bymex)
Thiazide (500-1000 mg IV chlorothiazide or 5-10 mg metolazone)
+/- Acetazolamide
+/- Fludrocortisone

May help stimulate the kidneys to secrete potassium
Primarily helpful in patients with mineralocorticoid deficiencies

Dialysis

Involve renal early because it takes a while to call in an HD nurse sometimes 
If no access and emergent HD is required → HD catheter placement

Strategies for suspected Brash syndrome

Epinephrine/Levo (if hypotensive/bradycardic)
Calcium gtt 

Disposition/wrap up

Many factors at play here – patient preference, access, degree of hyperkalmia, identifiable / corrected cause 

Take Home points

Hyperkelamia causes can be put into three categories, pseudohyperkalemia, due to redistribution, and due to total body increase in potassium. Check out the show notes for a more complete list
Hyperkalemia can be difficult to pick up on before the labs come back because it can lurk without symptoms or even ECG changes
If a patient does have ECG changes, they may not follow that linear pattern that is traditionally taught and ECGs can be poorly sensitive. Now, if you do see changes, the ones that are more commonly associated with adverse events are QRS widening, junctional rhythm, and bradycardia
Treatment is a numbers game, calcium for cardiac stabilization can last just 30-60 minutes, insulin will be the fastest way to shift potassium back into cells, but be mindful that 10 units is associated with increased episodes of hypoglycemia whereas 5 units may have the same effect in reducing potassium. And albuterol is at a much higher dose than what is given for asthma 
Lokelma is now a pillar of treatment for removal of potassium. 
Diuretics with the goal of kiuresis may have a role in the oliguric patient, and increased doses along with other agents may buy time in patients with severe hyperK when HD is not readily available 
Involve renal early if you think that the patient will require HD

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