Case
I’m calling from the ER and I have a 15-year-old female that has just been brought in by paramedics for a drug overdose. She is responsive to pain but non-communicative. This is her second suicide attempt according to the family. She lives with her grandparents and apparently they found her in her room surrounded by empty bottles of her grandfather’s heart medication. I’m not sure what she has taken but her heart rate is only 40 bpm. Her blood pressure is low at 92/50 and she responds to pain and stimuli but she’s non-communicative. I have poison control on the other line but given that there’s heart medication involved, I reached out to you as well. Any idea what I should do from here?
What am I thinking?
This call is unfortunately becoming all too common. My initial thoughts are focused on how to support the child and calling poison control in the event of an intentional ingestion is absolutely the right first call. We should start with supportive care of the patient and make sure that she is stable while following instructions from poison control. The next thought is to gain some understanding of the type of medication taken and how much was taken. Given the low heart rate and blood pressure, my concern is that of a calcium channel blocker or β-blocker overdose.
| Antiarrhythmic drug overdose | ECG findings |
|---|---|
| Digoxin | Scooping of ST segment |
| β-Blocker | Bradycardia, PR prolongation, AV block |
| Calcium channel blocker | Bradycardia, AV block, asystole |
| Sodium channel blocker | Widening QRS, ventricular arrhythmias |
| Potassium channel blocker | QT prolongation, AV block, Torsades de Pointes |
History and physical
A focused history is often required in the aftermath of an intentional ingestion patient with an emphasis on what may have been ingested. The ingested medications may be prescribed for the individual who took the overdose but may also be medications used by other family members as described in the scenario. Trying to determine what pills were taken and how much of them will provide a concentrated approach to treatment. Past medical history to include medication history and other medical diagnoses may help with drug–drug interactions and systemic findings such as renal or hepatic impairment. As treatment is focused on supportive care, physical exam would be concentrated on demonstrating hemodynamic stability. Frequent recording of the vital signs including heart rate and blood pressure with attention to perfusion of the extremities via pulse and capillary refill should be the key. With ingestion of antiarrhythmic drugs, any evidence for shock is likely to be cardiac in origin.
Diagnostic testing
Laboratory workup should include a blood and urine toxicology screen for any other substances that may have been ingested. Standard labs such as arterial blood gas, lactate, chemistry panel to look for blood glucose, electrolyte changes, and evidence for other organ damage such as the liver and kidneys should be obtained. In the case of a suspected or known digoxin overdose, a serum digoxin level should be obtained. An ECG should be obtained to determine any significant rhythm disturbance such as varying degrees of AV block or changes to the QRS, T waves, and QT prolongation. Ingestion of a β-blocker or calcium channel blocker may present in cardiogenic shock and an echocardiogram should be ordered to evaluate the myocardial function. Additional labs and tests may be required per poison control/toxicology recommendations.
Action plan
A plan of action is largely driven by the known exposure and clinical presentation of the patient. Consultation with poison control centers and adherence to their recommendations is of utmost importance. Common in all scenarios is the required careful observation of rhythm and patient hemodynamic stability. In all intentional ingestion cases, once toxicity is under control and hemodynamic stability has returned without concern for arrhythmias, psychiatric assistance is required. Long-term cardiac care follow-up is not required. All ingestions are a cry for help and require intensive treatment by a trained mental health specialist. The following highlights generally acceptable actions for encountered cardiac drugs in intentional ingestions. However, a common consideration for almost all ingestions of medications that can cause severe myocardial depression is the use of mechanical cardiac support such as extracorporeal membrane oxygenation (ECMO) or a ventricular assist device. The details of such treatment are beyond the scope of this book, but faced with a major overdose ingestion, the decision to call for help from advanced practitioners should be made as early as possible.
Digoxin
Digoxin toxicity may manifest with nausea, vomiting, hyperkalemia, hypokalemia, bradycardia, and/or tachyarrhythmias. A digoxin level, while helpful, may not predict toxicity as patients may manifest differently to varying levels. The ECG changes are characteristic of a “scooping” of the ST segment. Patients suspected of an intentional overdose of digoxin may benefit from a dose of activated charcoal though this should be cleared by toxicology experts. Patients should be admitted for observation under cardiac monitoring as toxicity usually peaks 6 hours after the last dose. Supportive treatment of bradycardia may involve cardiac medications such as atropine, isoproterenol, and/or rarely require cardiac pacing. Correction of potassium abnormalities may be beneficial in minimizing the effects of digoxin toxicity. Hyperkalemia can be treated with insulin that drives potassium into cells. Hypokalemia can also occur in patients who have vomiting or diarrhea. Hypokalemia should be corrected as it exacerbates the cardiotoxic effects of digoxin. In the setting of severe hemodynamic compromise due to bradycardia or ventricular arrhythmias, administration of antidigoxin Fab may be recommended by toxicology experts. Antidigoxin Fab has a high binding affinity for digoxin and removes it from sodium-potassium-ATPase thereby reducing its cardiac toxicity.
β-blockers
Initial treatment of β-blocker ingestion is supportive. Fluid boluses may be required to manage hypotension. Toxicology may recommend a dose of activated charcoal. Severe clinical presentation is primary hypotension, bradycardia, and cardiac dysfunction resulting in cardiogenic shock. Treatment of cardiogenic shock should be performed in an intensive care unit under the supervision and instruction of a poison control center/toxicologist assisted by critical care and/or cardiology. An accepted treatment for cardiogenic shock due to β-blocker ingestion includes the use of high-dose insulin euglycemic therapy, epinephrine, and phosphodiesterase inhibitors such as milrinone. As some β-blockers can have sodium channel blocking activity (propranolol), other clinical manifestations can include changes to QRS morphology, arrhythmia, and seizure activity. Treatment for sodium channel blockers will be reviewed in a later section.
Calcium-channel blockers
The initial treatment of calcium-channel blocker ingestion is largely supportive. Determination of the type of calcium-channel blocker will be an important distinction for clinical presentation and treatment. Many calcium channel blockers have sustained or extended-release formulations that could result in delayed toxicity. Calcium channel blockers such as verapamil or diltiazem have both cardiotoxic and vasodilatory effects while dihydropyridine calcium channel blockers (such as amlodipine) mainly cause vasodilation. Primary treatment may require activated charcoal. Intravenous fluids may be used to manage hypotension. For severe cases of hypotension and/or cardiogenic shock, administration of high-dose insulin euglycemic therapy along with chronotropic medications may be necessary under intensive care. For dihydropyridine ingestions, vasopressor medications such as norepinephrine may need to be utilized. Calcium infusion may be considered under the direction of intensive care and cardiology.
Sodium channel blocker
Sodium channel blocker toxicity manifests clinically as nausea, vomiting, and seizures. ECG findings demonstrated widening of the QRS and development of ventricular arrhythmia. Medications such as flecainide are difficult to manage as they have a high oral bioavailability and slow rate of elimination. Treatment involves administration of high-dose hypertonic sodium bicarbonate that increases sodium levels and results in serum alkalinization thereby offsetting the cardiotoxic effects of the drug. Given the high rate of ventricular arrhythmias, treatment should be held in intensive care units under strict cardiac monitoring. In rare instances, hemodynamic support in the form of extracorporeal membrane oxygenation may be required.
Potassium channel blockers
Potassium channel blockers result in QT prolongation that can set up for ventricular arrhythmias such as Torsades de Pointes or heart block. Continuous cardiac monitoring for arrhythmia disturbances is the mainstay of management for suspected potassium channel blocker overdose. For medications such as amiodarone, acute toxicity is a rare phenomenon given the large volume of distribution but lends to longer-lasting effects and therefore patients should be monitored for days after an ingestion. Beyond rhythm manifestations, patients may experience hypotension, nausea, dizziness, and headache. As with other medications, primary treatment with activated charcoal may be indicated to reduce gastric absorption. Serum potassium and magnesium levels should be monitored and maintained to avoid cardiac arrhythmias. Temporary pacing may be required for those patients in heart block. For patients in Torsades de Pointes, management consists of immediate cardioversion, magnesium, and acceleration/overdrive of heart rate by isoproterenol or with pacing. Serial ECGs should be obtained until normalization of the rhythm and QTc interval have occurred.
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