Inpatient / nephrology


Last Updated: 12/24/22

# Hyperkalemia

-- 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.

-- 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 ***.

-- 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

-- 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

Get Template PDF

PDF coming soon!

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

Trials and Literature

Other Resources