emDOCs Podcast – Episode 93: BRASH Syndrome

Today on the emDOCs cast we cover BRASH syndrome and what you need to know regarding diagnosis and treatment.


Episode 93: BRASH syndrome

 

Background:

  • Brash syndrome has 5 components: bradycardia, renal failure, AV nodal blocker, shock, hyperkalemia.
  • Patients at risk of renal insufficiency are the primary population, as well as those on certain medications:
    • AV nodal blockers: any of this class but specifically atenolol, nadolol, labetalol
    • ACE-I and ARBS: increase risk of hyperkalemia and renal dysfunction
    • Other medications that cause hyperkalemia: potassium sparing diuretics, digoxin, NSAIDs, trimethoprim, cyclosporin, tacrolimus
  • Older patients (more likely to have cardiac disease, chronic kidney disease, atherosclerosis)

 

Presentation:

  • Challenging to diagnose, especially in early stages of the disease.
  • The key is a patient who is on an AV nodal blocker and who has some sort of risk factor for renal insufficiency.
  • An inciting event will typically push them over the edge into BRASH syndrome:
    • Dehydration
    • Hypotension from sepsis or another condition
    • GI illness
    • Dosage increase of a chronic medication (e.g., beta blocker)
    • New medication (e.g., NSAID or potassium sparing diuretic)
  • Ask the following:
    • Is there mild hyperkalemia?  Is the patient taking a beta blocker or calcium channel blocker?  Is there some renal injury?  Is there a soft blood pressure?  If yes, consider BRASH.
  • Hyperkalemia does not typically cause severe bradycardia until the K is >8 mEq/L.  With BRASH, bradycardia typically occurs when K is only 5-7 mEq/L.
  • With BRASH, the major ECG change is mainly bradycardia and not all the typical hyperkalemia changes.

 

Management:

  • Four main keys to treatment (all concurrent):
    • Volume management
    • Treat bradycardia
    • Treat hyperkalemia
    • Correct underlying cause
  • #1: Volume management
    • Often challenging
    • May be fluid overloaded secondary to oliguric renal failure
    • Use history, exam, POCUS to determine fluid status
    • Target is euvolemia and serum bicarbonate of around 24 mEq/L.
    • If the patient is hyperkalemic and acidotic, administer isotonic bicarbonate (150 mEq of sodium bicarb in 1 L of D5W)
      • Recheck volume status and pH after this if they are still still volume down and acidemic, give another liter of isotonic bicarb; if fluid down but normal pH, give balanced crystalloid
      • Avoid normal saline, which will worsen non anion gap metabolic acidosis.
  • #2: Treat bradycardia
    • Calcium: 1 g calcium chloride or 3 g calcium gluconate IV; redosing is often necessary
    • Epinephrine: 5-10 mcg/minute
      • Will improve heart rate and shift potassium intracellularly
    • If still unstable after calcium and epinephrine, pacing will be needed
    • Skip atropine
  • #3: Treat hyperkalemia
    • If thinking BRASH, start hyperkalemia treatment (calcium, insulin/glucose, beta agonists)
    • First line medication is calcium
    • Can also use other hyperkalemia treatments:
      • Insulin/glucose
      • Albuterol if you haven’t started epinephrine
    • Consider diuresis only if euvolemic/hypervolemic 
      • IV furosemide/bumetanide
      • IV chlorothiazide
      • Acetazolamide 
      • Will need to match urine output with LR
    • If medication therapies are ineffective, the patient will need dialysis
  • #4: Treat the underlying cause
    • Stop AV nodal blocker
    • Treat any underlying infection 
    • If not improving with the therapies above and treating what you believe is the underlying cause, always consider primary overdose (beta blocker, calcium channel blocker, digoxin toxicity) and adrenal insufficiency
    • If considering adrenal insufficiency, give hydrocortisone IV

 

Summary:

  1. BRASH Syndrome has five components: bradycardia, renal failure, AV nodal blocker, shock, hyperkalemia.
  2. Can be challenging to diagnose, especially in early presentations.
  3. In someone with AKI, bradycardia, and hyperkalemia, think about BRASH.
  4. ECG change is mainly bradycardia, not all of the typical hyperkalemia changes.
  5. Bradycardia occurs at lower potassium levels than you would expect.
  6. There are four keys to management, which focus on treating all components of the syndrome.
  7. Remember to treat all components of the disease, including the underlying cause, once identified.

 

References:

  1. Farkas JD, Long B, Koyfman A, Menson K. BRASH Syndrome: Bradycardia, Renal Failure, AV Blockade, Shock, and Hyperkalemia. J Emerg Med. 2020 Aug;59(2):216-223. doi: 10.1016/j.jemermed.2020.05.001.
  2. Farkas J. BRASH syndrome: Bradycardia, Renal failure, Av blocker, Shock, and Hyperkalemia. Pulmcrit. Published February 15, 2016. 

 

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