Systemic toxicity from local anaesthetics occurs most commonly by inadvertent intravascular administration. All of the following statements are true EXCEPT:
Answer: D: Inadvertent intravascular administration is the most common cause of local anaesthetic systemic toxicity. This can occur infrequently during regional nerve blocks. In addition, systemic toxicity may occur in susceptible individuals such as patients with cardiac ischaemia, conduction abnormalities or heart failure, during intravenous or intraarterial administration at therapeutic doses. CNS symptoms generally precede cardiovascular effects in toxicity. If a patient develops any neurological symptom during or shortly after local anaesthetic administration, the patient should be closely monitored for development of cardiovascular toxicity bradycardia or other cardiac arrhythmias, hypotension, cardiovascular collapse and asystolic cardiac arrest. Bupivacaine is highly cardiotoxic therefore close attention is required during its use. Methaemoglobinaemia may occur following administration of lignocaine or prilocaine and is not dose related. Children are more susceptible to develop methaemoglobinaemia than adults after both local and topical administration.
Reference:
In which ONE of the following clinical situations may intravenous lipid emulsion (ILE) be a useful antidote?
Answer: A: ILE is a preparation used in parenteral nutrition and is currently being investigated as an antidote for toxicity secondary to highly lipid soluble drugs. The current recommendation for the use of ILE is for cardiovascular collapse or cardiac arrest secondary to local anaesthetic toxicity once adequate resuscitative measures have been initiated. It may also be considered in cardiac arrest refractory to standard resuscitative measures due to toxicity from highly lipid-soluble beta blockers and CCBs (such as propranolol and verapamil) and tricyclic antidepressants. Other beta-blockers and CCBs are not lipid soluble and therefore ILE is not indicated. The described mechanism of action for ILE is the formation of ‘a lipid sink’ where the intravascular lipid phase created by ILE sequester lipophilic toxins results in a reduction of the toxin concentration at the binding site.
References:
A patient presents to the emergency department (ED) with a history of deliberate ingestion of an unknown medication or substance. He appears agitated and confused with mydriasis, thirst, tachycardia, fever and urinary retention. He is likely to have ingested any of the following EXCEPT:
Answer: C: This patient has signs and symptoms consistent with anticholinergic syndrome. Common signs and symptoms of anticholinergic effects can be remembered with the mnemonic: Red as a beet, dry as a bone, blind as a bat, mad as a hatter, and hot as a hare.
The mnemonic refers to the symptoms of flushing, dry skin and mucous membranes, mydriasis with loss of accommodation, altered mental status (AMS) and fever or hyperthermia, respectively. Tachycardia and urinary retention are present.
All drugs mentioned, except digoxin, can lead to anticholinergic effects in overdose. Digoxin causes bradyarrhythmias, hypotension, nausea, vomiting and lethargy.
All of the following electrocardiogram (ECG) changes appear during major tricyclic antidepressant toxicity EXCEPT:
Answer: C: The most common ECG finding in tricyclic antidepressant (TCA) poisoning is sinus tachycardia, usually due to peripheral anticholinergic effects. TCAs block fast sodium channels in the myocardium and slow phase 0 depolarization of the action potential. Subsequently, ventricular depolarization is delayed, which leads to a prolonged QRS duration.
QRS complexes of more than 160 ms (four small squares) have a 50% chance of developing ventricular arrhythmias, whereas a QRS duration >100 ms (2.5 small squares on ECG), is associated with an increased risk of seizures.
Additionally, TCAs affect the right fascicle of the heart leading to right axis deviation. A large R wave in lead aVR is a highly sensitive screening tool for tricyclic antidepressant exposure. Furthermore, a high amplitude of this R wave has been associated with an increased risk of toxic effects. Data suggest that the finding of a large R wave in lead aVR may be even more predictive of seizure and arrhythmia than prolongation of the QRS complex. Liebelt et al found that an R wave of more than 3 mm in lead aVR was 81% sensitive and 73% specific for the development of seizures and arrhythmias.
Other ECG changes associated with TCA poisoning include:
When comparing venlafaxine and selective serotonin reuptake inhibitor (SSRI) overdose, which ONE of the following statements is TRUE?
Answer: B: Venlafaxine and desvenlafaxine are selective serotonin and noradrenaline reuptake inhibitors (SNRI). Seizures occur in 14% of patients with venlafaxine overdose but occur in <4% in SSRI overdose and are mainly associated with citalopram. Importantly, the onset of seizures may be delayed for up to 16 hours following overdose of venlafaxine. Therefore, all patients must be observed for at least 16 hours after ingestion with intravenous access in place. The risk of seizures is important to recognize in venlafaxine overdose. The patient who is at a high risk for seizures is anxious, sweaty, tremulous, tachycardic with mydriatic pupils and has clonus. Such patients should be prophylactically treated with intravenous benzodiazepines to control their tachycardia and this generally prevents seizures.
Cardiovascular toxicity is not common with either agent. Citalopram and escitalopram may cause dose dependent QT prolongation but torsades de pointes is rare. Minor dose-dependent QRS and QT prolongation may occur with venlafaxine overdose but seldom causes dysrhythmias. However, ingestion of very large doses (>7 g) of venlafaxine, may cause cardiovascular toxicity with hypotension and cardiac arrhythmias.
Mild serotonin syndrome may develop in some patients after a SSRI overdose. In both SSRI and venlafaxine overdose, severe serotonin syndrome occurs only if co-ingested with other serotonergic drugs.
Irrespective of the dose taken, the overdose of SSRI is usually not life threatening, whereas overdose with venlafaxine may be life threatening and is usually dose dependent.
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