Inpatient / nephrology

Hyperkalemia

Last Updated: 12/24/22

# Hyperkalemia

Checklist
-- Gut Check: 
repeat K (can check on blood gas) and see if hemolyzing due to high plt or WBC
-- ABCs: 
STAT EKG (look for peaked T waves, block, arrythmia) and give calcium gluconate; dialysis if severe and intitial temporizing efforts are ineffective
-- Chart Check: ***CKD, dialysis timing
-- Admission Criteria: ***
-- HPI Intake: *** missed dialysis, make urine, central access, new meds, symptoms (cramps, paresthesias, n/v/d), constipation
-- Can't Miss: *** EKG changes, acidosis
-- Admission Orders: *** continuous telemetry; low K diet; CBC, BMP, q2-4LFTs, VBG; consider CK, hemolysis labs, cortisol/aldo
-- Initial Treatment to Consider: In general treat the K if >6, rapid change, or symptoms including EKG changes - Insulin 10 units IV with D50 25mg; furosemide 40+mg IV, Lokelma 10mg TID; treat underlying cause - acidosis, hypovolemia, DKA, hypoaldo, remove meds, etc.

Assessment:
-- History: *** CKD, makes urine, missed dialysis, hyperpigmentation, FHx autoimmune dx
-- Clinical: ***muscle cramps, paresthesias, N/V/D, heart block
-- Exam: *** weakness, paresthesias, arrythmia
-- Data: *** EKG, ABG/VBG
-- Etiology/DDx: *** AKI/CKD, drugs (BB, calcineurin inhibitors, ACE/ARB, NSAIDs, spironolcatone, bactrim), acidosis, hypoaldo/primary adrenal insufficiency, cell lysis (rhabdo, TLS), transfusion reaction, decreased insulin, type IV RTA

The patient's HPI is notable for ***. Exam showed ***. Labwork and data were notable for ***. Taken together, the patient's presentation is most concerning for ***, with a differential including ***.

Plan:
Workup
-- Monitor: *** Trend K q *** and EKG q ***; Continuous telemetry
-- Consult renal if c/f dialysis need (unable to temporize with EKG changes or sxs)
-- Consider sending CK, hemolysis labs (LDH), cortisol/aldo/renin

Treatment
-- Calcium gluconate 1g IV q hour while remaining hyperkalemic; repeat 5min PRN (lasts 30-60 mins)
-- Temporizing: *** Insulin 10 units IV with D50 25mg if BG <250; bicarb amp if pH <7.2
-- Eliminate: *** furosemide 40+mg IV, sodium zirconium (Lokelma) 10mg TID; dialysis if symptoms, EKG changes, unable to lower by other means
-- Low potassium diet
-- If c/f Adrenal Insufficency - hydrocort 15-25mg split 2-3 doses + fludrocort 0.05-0.2 daily

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If You Remember Nothing Else

The most common cause of hyperkalemia presenting to the hospital is from ESRD (missed dialysis) and medications. Get an EKG and give calcium gluconate if K >6. You should give insulin 10 units with D50 25mg (if BG <250) if need to temporize and then lasix 40mg+ IV and/or lokelma 10mg TID to eliminate the K. Don't wait to see if elimination will work if there is an indication for dialysis - just do it.

Clinical Pearls

  • In vivo hemolysis is a genuine cause of hyperkalemia, whereas hemolysis in vitro either while collecting a sample or while waiting to be run is pseudohyperkalemia
  • Etiologies of hyperkalemia can be separated into Redistribution Process vs Decreased Excretion
  • Hyperkalemia from acute insults is usually short-lived unless the process is ongoing (hypoaldo, medications, etc.) or renal function is impaired and unable to excrete K
  • K is exchanged for Na in the distal nephron - if RAAS on (hypovolemia, CHF, cirrhosis), less Na makes it to this portion, and K is not excreted in exchange for the Na 
  • The resting membrane potential is ~90 mV, this is lower when there is more K outside cells which means less signal is needed to fire an action potential, leading to increased excitability and possibly arrhythmias, especially in an acute setting
  • Calcium gluconate should reverse EKG changes in 5 minutes, if not, push again
  • Tempporizing and redistributing K can drive the K down ~0.5-1.5 in the short term
  • Elimination via furosemide or Lokelma requires urine or stool output, otherwise will need to dialyze
  • The EKG does not always correlate with the actual K level - it depends in part on the chronicity of the elevation
  • EKG progression - peaked T waves → increased P interval, flattening of P wave → wide QRS and BBB → sine wave → PEA/asystole/VF
  • Atria are more susceptible to K, and will see p-wave flattening earlier than changes in QRS
  • Remember that in DKA will be hyperkalemic since insulin is not present to push into cells, but TOTAL body K will be low, so you need to replete when less than 5.2 and hold insulin if less than 3.3
  • Hypo/Hyperkalemia is one of the H’s in the H’s and T’s for causes of PEA arrest; at very high levels can lead to asystole - never a bad idea to give calcium gluconate if there is a suspicion
  • Typically outpatient medicines like ACE/ARB, spironolactone, and Bactrim can all cause hyperkalemia
  • Acidosis causes hyperkalemia by messing with Na/H antiporter efficacy which leads to decreased intracellular Na, which impacts the efficacy of the Na/K-ATPase, and leads to increased extracellular K, leading to hyperkalemia
  • Typically outpatient medicines like ACE/ARB, spironolactone, and Bactrim can all cause hyperkalemia
  • Some of the most common sources of dietary K+ are potatoes, cereals (bran products, granola), meat, and dairy (milk, yogurt). Other potassium-rich foods include avocados, bananas, leafy green vegetables (except for kale), root vegetables (beets, carrots), and tomatoes
  • Type IV RTA leads to reduced ability to reabsorb sodium in the distal tubule, thus less K excretion

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