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--- beta_blocker_toxicity [2025/01/07 17:39] – jkohts
+++ beta_blocker_toxicity [2025/01/07 19:45] (current) – jkohts
@@ Line 121: / Line 121: @@
 ==== - Respiratory effects ====
 **Bronchospasm**\\
-β-blocker overdose can result in bronchospasm as a result of β2 antagonism, particularly in individuals with underlying reactive airway disease. It is unlikely
+β-blocker overdose can result in bronchospasm as a result of β2 antagonism, particularly in individuals with underlying reactive airway disease.
 ==== - Metabolic effects ====
@@ Line 130: / Line 130: @@
 <code>
-Need to check this - never seen this elsewhere:
+Two problems here.
+(1) The above are contradictory.
+(2) Need to check this - never seen this elsewhere:
 There are some reports of patients responding to glucose with “normal” blood glucose measurements. Therefore, it is worth giving a bolus of 50% glucose to any patient with CNS effects.
 </code>
@@ Line 176: / Line 179: @@
 ==== - Supportive ====
-IV access with IV fluids (normal saline) should be secured as soon as possible. ECG monitoring in intensive care is indicated for all but the most trivial propranolol or sotalol poisonings. Glucose should be given to any patient with decreased consciousness or seizures regardless of a normal blood sugar.
+IV access and IV fluid resuscitation (with normal saline or balanced crystalloid) should be initiated. ECG monitoring in intensive care is indicated for all but the most trivial propranolol or sotalol poisonings. Glucose should be given to any patient with decreased consciousness or seizures regardless of a normal blood sugar.
+<code>
+Again the empirical glucose administration needs to be checked.
+</code>
 ==== - Decontamination ====
-Syrup of ipecac should not be used to decontaminate beta-blocker poisonings under any circumstances. Gastric lavage should be considered in large ingestions of propranolol or sotalol if patients present within one hour of ingestion. Atropine should be given prior to lavage and in any patient who is vomiting. Oral activated charcoal should be given to all patients ingesting any overdose of a beta-blocking drug who present within 2 hours.
+**Gastric lavage** should be considered in large ingestions of propranolol or sotalol if patients present within one hour of ingestion. Atropine should be given prior to lavage and in any patient who is vomiting.
+**Oral activated charcoal** should be given to all patients ingesting any overdose of a β-blocking drug who present within 2 hours.
+**Whole bowel irrigation** may be considered in patients who have ingested sustained-release preparations.
+**Induction of emesis** (e.g. with syrup of ipecac) is __contraindicated__ in β-blocker toxicity due to risk of airway compromise (from aspiration and reduced consciousness) and vagal stimulation which may worsen bradycardia.
 ==== - Enhanced elimination ====
+The drugs that are water soluble are predominantly renally cleared, namely sotalol and atenolol. Among these drugs, sotalol has significant 'antiarrhythmic' effects (via K+ channel blockade) and frequently causes life-threatening poisoning.
-The drugs that are water soluble are predominantly renally cleared. Among these drugs, only sotalol has significant “antiarrhythmic” effects and frequently causes life threatening poisoning. Thus, haemodialysis is unlikely to be useful except perhaps for sotalol in patients with life threatening toxicity and impaired renal function.
+Extracorporeal treatment with renal replacement therapies (intemittent hemodialysis preferred) can be considered in patients who have all of the following [(34112223>[[https://pubmed.ncbi.nlm.nih.gov/34112223/|PMID: 34112223]]. Bouchard J, Shepherd G, Hoffman RS, et al. Extracorporeal treatment for poisoning to beta-adrenergic antagonists: systematic review and recommendations from the EXTRIP workgroup. Crit Care. 2021;25(1):201. Published 2021 Jun 10. doi:10.1186/s13054-021-03585-7)]:
+  * Sotalol or atenolol toxicity
+  * Significant renal impairment
+  *__Refractory__ cardiotoxic effects (bradycardia, hypotension, recurrent polymorphic VT)
+<code>
+I have removed the argument where sotalol is the only one which should be dialyzed, in light of ExTRIP recommendation to consider atenolol also. - Review to keep changes.
+</code>
 ==== - Antidote ====
-There are a number of drugs that will antagonize some of the cardiac effects of beta-blockers. All these treatments may be used simultaneously, if this is required
+There are a number of drugs that will antagonize some of the cardiac effects of beta-blockers. All these treatments may be used simultaneously if required.
+  * Atropine
+  * Glucagon
+  * Isoprenaline
+  * Dextrose & Insulin
-<code>
+**Atropine**\\
-  Atropine
+This should be tried in all patients with bradycardia. It should be given prior to intubation, lavage, or any other procedure that might increase vagal tone and in patients who are nauseated or vomiting.
-  Glucagon
-  Isoprenaline
-  Dextrose & Insulin
-</code>
+**Glucagon**\\
+IV glucagon had been used as antidote for beta-blocker poisoning in the past but its use has been largely superseded by HIET. Glucagon increases intracellular cAMP and activates myosin kinase independent of β-receptors.
+\\
+  * 💊 **Glucagon** IV 5-10 mg as a bolus, then an IV infusion titrated against heart rate and blood pressure (starting at 5-10 mg/hour, or the 'reponse dose' per hour).
-Atropine \\ This should be tried in all patients with bradycardia. It should be given prior to intubation, lavage, or any other procedure that might increase vagal tone and in patients who are nauseated or vomiting.
+**Isoprenaline** \\
+Isoprenaline is a non-selective competitive β-agonist. Doses should also be titrated against cardiac parameters and the dose required may be ten or twenty fold larger than normally used. As both the agonist and antagonist are competing for the same receptors, much larger doses are needed to reach the same level of receptor occupancy. Dose requirements will fall rapidly as the β-blocking drug is metabolised.
-**Glucagon** \\ Glucagon had been used as antidote for beta-blocker poisoning in the past but its use has been largely superseded by insulin dextrose. The rationale for its use is that it increases cyclic AMP and activates myosin kinase independent of beta-receptors. The dose is 5 - 10 mg IV as a bolus and then an infusion titrated against heart rate and blood pressure (starting at 5 - 10 mg/hour).
-**Isoprenaline**  This is a non-selective competitive beta agonist. Doses should also be titrated against cardiac parameters and the dose required may be ten or twenty fold larger than normally used. As both the agonist and antagonist are competing for the same receptors, much larger doses are needed to reach the same level of receptor occupancy. Dose requirements will fall rapidly as the beta-blocking drug is metabolised.
+**HIET**\\
+Patients who require inotropics support should be commenced on Dextrose & Insulin. This should be implemented in patients not responding to isoprenaline.
-Patients who require inotropics support should be commenced on Dextrose & Insulin.
+<code>
+This section has been reworked 08/01. Goldfrank's has a discussion of calcium, general catecholamines (other than isoprenaline), and lipid emulsion.
+Do we want to include those in?
+Also, in what order should we include them?
+</code>
-This should be implemented in patients not responding to isoprenaline.
 ==== - Treatment of specific complications ====
-Seizures Glucose should be given regardless of a normal blood sugar. Otherwise, they should be treated conventionally with benzodiazepines(eg diazepam). If seizures are refractory-use phenobarbitone.
+**Seizures**\\
+Glucose should be given regardless of a normal blood sugar. Otherwise, they should be treated conventionally with benzodiazepines (eg diazepam). If seizures are refractory, use phenobarbitone.
+<code>Why phenobarb instead of usual status epilepticus protocol?</code>
-Arrhythmias Ventricular tachycardia (torsades de pointes) may occur with sotalol or occasionally propranolol. Conventional treatment is with magnesium, isoprenaline, or cardiac pacing. Magnesium has calcium channel blocking effects and is potentially hazardous as it may further impair cardiac conduction and contractility. It should be used with great caution if at all. Isoprenaline or cardiac pacing to achieve a heart rate of 120-140 bpm is the safest option.
+**Arrhythmias**\\
+Ventricular tachycardia (polymorphic VT, torsades de pointes) may occur with sotalol or occasionally propranolol. Conventional treatment is with magnesium, isoprenaline, or cardiac pacing. Magnesium has calcium channel blocking effects and is potentially hazardous as it may further impair cardiac conduction and contractility. It should be used with great caution if at all. Isoprenaline or cardiac pacing to achieve a heart rate of 120-140 bpm is the safest option.
+<code> Unsure about this due to very high target HR, and probably should caveat with needing invasive BP monitoring? </code>
 ==== - Observation/disposition ====
 ===== - Prognosis =====
+Occasional late complications/deterioration have been reported generally in patients who have had significant poisoning. It is likely that these relate to too rapid withdrawal of treatment. Long term sequelae have not been reported and no follow up is required after resolution of the clinical signs or ECG findings, unless the patient has been profoundly hypotensive.
-Occasional late complications/deterioration have been reported generally in patients who have had significant poisoning. It is likely that these relate to too rapid withdrawal of treatment. Long term sequelae have not been reported and no follow up is required after resolution of the clinical signs - ECG findings unless the patient has been profoundly hypotensive.
 ===== - References =====