Emergency Case Challenge: After Argument, Unresponsive Woman Found By Her Boyfriend

Gregory Taylor, DO; Jacklyn McParlane, DO

Disclosures

September 19, 2022

The differential diagnoses are numerous. Patients often ingest multiple medications, each presenting a unique character profile, adding to the complexity of the clinical presentation. Some of the most common overdoses encountered can appear to mimic a CCB overdose.

Tricyclic antidepressant (TCA) overdose presents in similar ways to a CCB overdose; however, some differences are noted. As a sodium-channel blocker, a TCA overdose may present with seizures and ventricular dysrhythmias. An EKG often reveals a QRS duration > 100 ms, with an associated R wave in aVR. In the patient in this case, the QRS duration was within normal limits, and no R wave was noted in aVR. In general, a QRS < 100 ms is not usually associated with any significant toxicity; however, in patients with a QRS > 100 ms, the risk for seizure is roughly 33%. With a QRS > 160 ms, approximately 50% of patients have ventricular dysrhythmias.

TCAs are unique in that they do not only exhibit sodium-channel blocking effects but also exhibit anticholinergic effects (eg, dilated pupils, dry and hot flushed skin, tachycardia, decreased/absent bowel sounds, urine retention), antihistamine effects (sedation), and alpha-blockade effects (vasodilation/hypotension). Treatment modalities include the administration of one ampule (50 mEq) of IV bicarbonate at a time, until the QRS narrows, and then starting a continuous infusion.

Beta-blockers can also mimic a CCB overdose but may also be co-ingested. Two specific beta-blockers require special recognition: propanol, which causes sodium-channel blockade that results in widening of the QRS, and sotalol, which causes potassium efflux blockade that results in a long QT and torsades de pointes.[4] Beta-blocker overdose may result in hypotension, bradycardia, heart failure, hypoglycemia, hyperkalemia, seizures, and coma. Management of beta-blocker overdose is similar to CCB overdose management, involving pressors and high-dose insulin; however, clinical research has shown that giving an initial glucagon bolus (0.1 mg/kg IV) and assessing for an MAP ≥ 65 mm Hg. A glucagon drip is then initiated at 0.1 mg/kg/hr IV. If MAP remains < 65 mm Hg, proceed to pressors and high-dose insulin therapy.

Digoxin toxicity also shares some similar characteristics to CCB toxicity. Digoxin is often used to increase cardiac output through positive inotropic activity by inhibiting the Na/K ATPase. Bradycardia, hypotension, and hyperkalemia are often present in digoxin overdose. Hyperkalemia becomes the most important predictor of outcome, with a mortality rate in untreated patients approaching 100% when the potassium level is > 5.5 mEq/L. Patients often present with signs of an overdose within 1-2 hours, with nausea, vomiting, and abdominal pain. They may also describe yellow vision. In severe cases, the patient progresses to AV nodal blockade and ventricular fibrillation. Treatment is aimed at correcting the hyperkalemia and administering digoxin antibody.

Clonidine is a central-acting alpha-2 agonist with various uses, ranging from blood pressure control to alcohol, nicotine, and narcotic withdrawal. Symptoms often resemble an opioid overdose, with bradycardia, hypotension, respiratory depression, miosis, and eventual coma. Patients on clonidine who appear comatose may awaken with lucid intervals when physical/verbal stimuli are used, compared with opiate overdose, where the same stimuli result in the patient continuing to be obtunded. Treatment is largely supportive, with some evidence for naloxone because it improves the mental status of adult and children who have significant clonidine toxicity; however, the absolute benefits are unproven.

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