In this episode, I’ll discuss which beta-blockers should be dialyzed to treat toxicity.
Beta-blocker toxicity is often severe, causing bradycardia, hypotension, and cardiogenic shock. Beta blockers are responsible for a sizeable portion of fatal poisonings in the US.
Supportive therapy is the mainstay of care. Treatments like high-dose insulin euglycemic therapy, glucagon, and vasopressors are used to treat cardiogenic shock and allow the patient to metabolize or clear the toxic levels of beta-blockers. Howver, many commonly used beta-blockers are dialyzable to some degree.
The EXtracorporeal TReatments In Poisoning (EXTRIP) workgroup is a body of experts that exists to provide recommendations on the use of extracorporeal treatments in poisoning, and recently published a systematic review of dialysis in beta-blocker toxicity in the journal Critical Care.
While the mechanism of action is the same, beta-blockers as a class of medications are quite heterogenous, with some requiring renal adjustment and some having either large or small volumes of distribution or protein binding capacity.
For the review, 76 studies were analyzed which represented over 300 patients. Toxicokinteic data was available for atenolol, propranolol, and sotalol.
The workgroup’s recommendations for each medication were at times different depending on whether or not the patient had chronic renal insufficiency.
For example, in patients severely poisoned with atenolol and kidney impairment who also have refractory bradycardia and hypotension, dialysis was recommended. But in patients severely poisoned with atenolol and without kidney impairment, no recommendation could be given.
The panel made a similar recommendation for sotalol poisoning – when refractory bradycardia and hypotension and/or recurrent torsade de pointe are present in a patient who also has kidney impairment, dialysis was recommended. No recommendation could be made if kidney impairment is not present. In addition, the guideline authors suggest against performing dialysis in a patient with sotalol toxicity solely based on the QT interval.
Owing to ample data as well as its small volume of distribution, in all patients severely poisoned with propranolol the workgroup recommended against performing dialysis.
There are considerable research gaps with the other beta blockers, and the possibility exists that dialysis might be indicated on a case-by-case basis, however there was not enough data for the workgroup to make firm recommendations. Should a unique case come up, Table 1 of the article contains references and physicochemical properties and pharmacokinetics of immediate-release β-adrenergic antagonists that could be used to help make patient-focused decisions on the utility of dialysis in the abscense of higher quality data.
Once dialysis is initiated to treat beta-blocker toxicity, the workgroup recommends that rather than a target serum concentration, clinicians should use heart rate, blood pressure, end-organ perfusion, presence of torsades, and vasopressor requirements to help guide the duration of therapy.
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