Not a lot of people have heard of BRASH syndrome, as it's really only been recognised as it's own thing in the last three or four years, so we decided to do a little post on it here, with the key bits you need to know.

Sound familiar?

An elderly patient presents seriously but non-specifically unwell to ED. They're on a standard cocktail of meds including a statin, beta blocker, ACEi and maybe something bleedy for their atrial fibrillation.

They report being a bit 'off' for a few days, maybe not drunk enough and now they're headed for multiple organ failure with AKI, hypotension, bradycardia, high potassium (but not really enough to cause all this badness) and general everything-shutdown.

Classic BRASH syndrome.

Here's what happens

• You start with some injury or insult that causes renal injury
• This causes hyperkalaemia and also build up of the AV blocking drug
• Together these work synergystically to cause bradycardia and reduced cardiac output
• This leads to shock
• This worsens the renal failure

Oh look a spiral of terribleness.

So who gets it?

Well unsurprisingly it's people on AV node blocking drugs who get an unexpected bout of AKI.

Examples include

• older patients
• with infections
• on diuretics
• in the summer
• who've been vomiting
• or had a recent dose change in their ACE inhibitor

Why didn't we know about it before?

Well we sort of assumed something else was going on and treated that instead.

Sometimes the patient got better by accident, and other times we missed it.

Usually there's fairly good-going hyperkalaemia, which we know how to recognise and for which we have a defined treatment pathway, so there's often a knee-jerk response as soon as the first gas comes back.

So most cases of BRASH end up getting diagnosed as hyperkalaemic AKI and left at that.

This isn't the worst thing in the world, as most of the treatment for BRASH is usually covered by treating hyperkalaemia properly, but it's important not to forget the fact that there's some nodal naughtiness going on in the shadows.

So how do I fix it?

• Fluid resuscitation (unless overloaded, such as cardiorenal syndrome)
• IV calcium (to stabilise the membrane)
• Insulin and dextrose (to shift the potassium)
• Salbutamol nebulisers (helps with the potassium and the bradycardia)
• Furosemide 80-160mg (to offload potassium)
• Renal replacement therapy (if not responding to furosemide)
• Fludrocortisone can help offload potassium (especially if on anything inhibiting aldosterone like ACE/ARB/spironolactone)

Remember calcium!

This is probably the key take home message here - look at the resus council guidelines for bradycardia with a pulse.

A patient with BRASH syndrome is likely to be seriously bradycardic but still vaguely pulsatile, and you may well find yourself meandering down this flow chart and never actually manage the hyperkalaemia that's causing the whole problem in the first place.

Some solid tweets

Further reading and references

PulmCrit- BRASH syndrome: Bradycardia, Renal failure, Av blocker, Shock, Hyperkalemia

This is one of my favorite diagnoses. When first encountered, it may seem bewildering and difficult to treat (1). Indeed, standard ACLS algorithms often fail with these patients. However, once understood, this disorder is easily treated and patients typically improve rapidly.

EMCrit ProjectJosh Farkas

BRASH syndrome

BRASH syndrome is an acronym for Bradycardia, Renal Failure, AV blockade, Shock, and Hyperkalaemia. BRASH syndrome is a synergistic process created by a combination of hyperkalaemia and medications blocking the atrioventricular (AV) node. The most common precipitants are hypovolaemia and medications promoting hyperkalaemia or renal injury. BRASH syndrome is fundamentally a synergistic process created by […]

Life in the Fast Lane • LITFLTom Cassidy and Mike Cadogan