One Pill Can Kill: The Case of The Cough Killer
The Case
The town is hopping with university students as Freshman Week festivities enter what seems will be a ferocious weekend. Last night, you carried three intoxicated first years out of bars and clubs and you expect tonight will be no different. Maybe even worse.
It’s just past midnight, and you’re off on a call, this time to a party in an apartment across the road from the main university dormitory. Another freshman passed out. The music is still pumping when you and two police officers exit the elevator and follow the decibels to the apartment at the end of the hall.
There must be two dozen partiers inside. Empty bags of chips litter the kitchen counter, and a boy who looks to be 16 or 17 is laying on the linoleum floor of the tiny galley. He’s cyanotic and has drool pooling on the floor.
Your posture immediately changes, and you leap to his side and check for a pulse. Nothing. You direct a police officer to start CPR while you clear a space in the living room where you can work the arrest. Not even a minute later, and you’ve dragged him into the center of the room. Your partner starts BVM ventilation and reports easy compliance while you attach the defibrillator. Your heart sinks as you see an ugly sine wave; wide, short-amplitude, and very slow.
Your mind races with a differential diagnosis for pulseless electrical activity. You run the list of H’s and T’s and nothing seems obvious. It could be hyperkalemia, but why him, why now? It must be an overdose. But of what?
Differential Diagnosis of Pulseless Electrical Activity (PEA): Hs and Ts
- Hypoxia
- Hypovolemia
- Hydrogen ions (acidosis)
- Hyperkalemia
- Hypothermia
- Anaphylaxis
- Toxins
- Tamponade
- Tension pneumothorax
- Thrombus (coronary, pulmonary)
- Trauma
The other police officer, who is corralling the onlookers, suddenly shouts, “Hey medic, listen to this!”
He pushes a young girl to the front of the crowd.
“We were taking cough medicine to get high. He took an awful lot,” she says through tears.
Cough Suppressants Containing Benzonatate:
Dextromethorphan is a common ingredient in cough syrups and its abuse has been on the rise. Available over the counter, the effects are often compared to ketamine and PCP, both dissociative anesthetics. Often mixed with acetaminophen, it can be a dangerous toxin.
But this case isn’t about dextromethorphan. Another cough suppressant is responsible for this cardiac arrest: benzonatate. Benzonatate (Brand names: Tessalon Perles or Zonatuss) has an FDA warning that accidental ingestion in children can cause death.
Like tricyclic antidepressants, some cardiac antidysrhythmics, and cocaine, benzonatate is a sodium channel blocker. It presents as a wide complex rhythm and can degrade into ventricular tachycardia. Because it poisons sodium channels, defibrillation is rarely successful.
The treatment for sodium channel toxicity is to push sodium—lots of sodium. This can lead to normalization of ECG abnormalities right in front of your eyes. If you carry sodium bicarbonate, this would be a good time to push it. In my career, I’ve called for extra ALS backup to bring me more amps of bicarb; each 50mL vial contains 23mg of sodium; that’s eight times the amount of sodium as you’ll find in a liter bag of 0.9% saline. Increasing serum sodium can allow some resumption of sodium channel functioning.
In the ER, we’ll often push lidocaine, another sodium channel blocker, because it has very high affinity for cardiac sodium channels. It can bump toxic sodium channel blockers off the receptor. So, you change one blocker for another, right? Sodium may have a high affinity for receptors, but it doesn’t like to hang out. If benzonatate wants to date, lidocaine wants a one-night stand. It kicks the toxin off the channel and then leaves, allowing sodium influx.
Other salvage therapies include intralipid fat emulsion and extracorporeal membrane oxygenation.
Back to the Case
The police officer returns with empty benzonatate packets. Dozens of liquid-gel capsules are missing. You’ve given epinephrine twice and figure it’s time to try bicarb; you may need to touch base with your medical director. If authorized, you’re likely going to get an order to give all your sodium bicarb—whatever is in your bag and in your truck. You may also get an order to trial a bolus of lidocaine.
After 17 minutes of CPR, 4 amps of epi, and 6 amps of bicarb, you see ventricular fibrillation. You administer 200J of energy and resume CPR. You see your EtCO2 start to climb from 9 mmHg to 23 mmHg and see QRS spikes through the CPR artifact. You pause CPR, check a pulse, and breathe a sigh of relief: Return of spontaneous circulation (ROSC).
Citation:
https://pmc.ncbi.nlm.nih.gov/articles/PMC3526931/
Blair Bigham worked for a decade as a flight paramedic on four continents, a job he misses every day. He is now an ER and ICU physician at the University of Toronto and a public health researcher at the Dalla Lana School of Public Health. @BlairBigham blairbigham.com
