
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
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- Antibiotics: Bactrim, antifungals
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- 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
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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