Regarding acute digoxin toxicity, which ONE of the following statements is CORRECT?
Answer: D: Predictors of potentially lethal acute digoxin toxicity are:
Any hyperkalaemia is significant in acute digoxin toxicity and is an indication for the use of digoxin immune Fab as a temporizing measure.
Temporizing options for hyperkalaemia treatment, while awaiting Fab, are sodium bicarbonate intravenously as a bolus and insulin-dextrose treatment. When treating severe hyperkalaemia in acute digoxin toxicity, calcium gluconate should not be used as a membrane stabilizer as it may worsen the cardiotoxicity.
Some patients may have taken digoxin with other cardiotoxic drugs or the initial history of the digoxin overdose may not have been available. In such patients a therapeutic trial of digoxin immune Fab may be helpful.
Serum digoxin levels are not clinically valuable after the patient had digoxin immune Fab as laboratories typically measure both bound and unbound digoxin resulting in very high serum levels.
Reference:
Which ONE of the following statements regarding the use of digoxin immune Fab (Digibind) is INCORRECT?
Answer: A: Digoxin immune Fab is a life-saving antidote in both acute and chronic digoxin toxicity. They are fragments of IgG antibody molecules against digoxin produced in sheep. These molecules bind directly to intravascular and interstitial digoxin and 1 ampoule of Fab binds 0.5 mg of digoxin. The appropriate Fab dose can be calculated using the ingested dose of digoxin in acute toxicity or steady state serum digoxin level in chronic toxicity. However, in clinical practice empiric doses are often used in suspected patients.
Suggested empiric doses in acute toxicity are:
Then, repeat 5 ampoules every 30 minutes until the reversal of toxicity.
The suggested empiric dose in chronic toxicity is 2 ampoules initially. Then, repeat 2 ampoules every 30 minutes until the reversal of toxicity. Five ampoule can be administered in a cardiac arrest.
Treatment of patients with chronic digoxin toxicity with non-life-threatening features with immune Fab is cost effective. Non-life-threatening cardiac arrhythmias and moderate–severe gastrointestinal symptoms should be treated, especially in patients with renal impairment.
The end points of treatment in any situation are the return of normal cardiac conduction and rhythm and resolution of gastrointestinal symptoms.
A 4-year-old otherwise healthy child presents with severe toxicity due to accidental overdose of a calcium channel blocker (CCB) drug.
Which ONE of the following statements is FALSE?
Answer: D: Severe toxicity secondary to CCB drug ingestion is due to:
These result in hypotension and bradydysrythmias with profound cardiovascular collapse.
The non-dihydropyridine CCBs are verapamil and diltiazem. Verapamil has moderate effects on both cardiac conduction and vascular smooth muscle tone in therapeutic dosage. These effects are exaggerated in toxic dosages of verapamil, especially in toddlers, with resultant hypotension and bradydysrythmias. Additionally, verapamil is the most potent negative inotropic of all CCB, and causes equal depression of heart contraction and vascular smooth muscle dilation at any concentration with subsequent profound hypotension. In children, initially there may not be any specific clinical features that could indicate severe toxicity. The most common clinical effect is altered mental status.
The dihydropyridine CCBs include nifedipine, amlodipine, felodipine and the most newer agents. They bind more selectively to vascular smooth muscle calcium channels than to cardiac calcium channels. Therefore, in mild to moderate overdoses these CCBs can cause reflex tachycardia secondary to relative hypotension caused by the lax vascular smooth muscle. This is not a feature in severe toxicity and these agents may cause complete heart block, depressed myocardial contractility and vasodilation, which ultimately results in cardiovascular collapse.
Severe CCB toxicity may lead to hyperglycaemia because a reduced release of insulin from pancreatic islet cells.
References:
Regarding beta-blocker overdose, which ONE of the following statements is TRUE?
Answer: A: Isolated overdose with a beta-blocker, except sotalol and propranolol, causes minimal or no toxicity in most healthy adults. The risk of toxicity is increased in patients with underlying cardiovascular disease, those who take other potential cardiotoxic drugs and in the elderly.
Overdoses with sotalol and propranolol are serious and potentially harmful to adults. Similarly, the risk of toxicity is high if even 1–2 tablets of sotalol or propranolol are taken by a child, whereas this risk seems to be minimal in children ingesting other beta-blockers.
The onset of features of toxicity usually occurs early within a few hours unless due to sustained release formulations. PR interval prolongation on ECG with or without bradycardia is the earliest sign of toxicity.
Regarding management of severe toxicity due to a deliberate overdose of sotalol, which ONE of the following statements is TRUE?
Answer: C: Sotalol toxicity can cause QT prolongation leading to polymorphic VT (torsades de pointes). Patients who manifest torsades de pointes can be treated with intravenous magnesium initially and then be started on an isoprenaline infusion. Patients who do not respond to the above will require overdrive pacing. Bradyarrhythmias, including sinus bradycardia, junctional rhythms and all heart blocks, and hypotension are the other significant cardiovascular issues. An initial fluid load is important in these patients. Atropine can be used as a temporizing measure for bradycardia. Isoprenaline or adrenaline intravenous infusion should be considered for persistent bradycardia and hypotension.
Propranolol toxicity and not sotalol toxicity causes QRS widening (similar to tricyclic overdose) therefore will require NaHCO3 to control ventricular arrhythmias. Additionally, Propranolol toxic patients often require early intubation and ventilation, whereas this is a less likely scenario in sotalol overdose.
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