Critical Care Toxicology: What Did My Patient Take? 1/2

Surprisingly, patients aren’t entirely truthful about what they may have ingested to make them sick. Or, they might be in a state where they can’t share the information due to their medical condition. This can put the medical team in a worse case scenario where if they knew what the patient took . . . they might be able to offer the right antidote.

Without the information it can seem like a shot in the dark to try and reverse the effect the substance is having on the individual.

Recently, I heard a fascinating lecture given by a doctor of toxicology who gave some guidelines, based on the patient’s signs, as to what that drug might be and I thought I’d share them with you for some great writing details.

Let’s first assume that we at least know the patient likely ingested something. They’re discovered by EMS in their home with an array of alcohol, pills, and drug paraphernalia. A good EMS team will try and take stock of what they see and report to the ER what they found. They’ll likely not grab illegal drugs like weed or powders (this would be for the police to confiscate) but they may bring unidentified pills and prescription bottles to help us. This can help narrow down what the person might have taken.

The opposite is finding someone unconscious in the middle of the street with nothing around them and the police call EMS for transport.

Or, even better, a teen has been involved in a “pharming party” where they raid every medicine cabinet they have access to and dump all they find into a punch bowl. Then proceed to swallow a handful of these pills with a bunch of alcohol. I have had cases like this where EMS grabbed the bowl and brought it with them. I mean, a punch bowl filled with prescription drugs but no boxes or labels. Even if we have the pills– it takes time to identify what they might be.

Time the patient might not have.

Scenario #1:

The patient presents with low heart rate and low blood pressure.

First, why would we think this may be a drug ingestion? The body’s normal response to low blood pressure is to increase your heart rate– not lower it– as a mechanism to prevent shock.

There’s only one other medical state I can think of that would mimic this and that would be a spinal cord injury. When the spinal cord is damaged, you lose nerve innervation that would help increase blood pressure. So, in absence of a traumatic event, a spinal cord injury would be ruled out. However, an unconscious person can’t tell us if they’ve been injured which further complicates the picture.

Drugs that can create this picture could be the following:

1. Beta-blocker. Your heart has beta receptors. When these are stimulated, say by a release of adrenaline in your body, the heart contracts harder and beats faster. A beta-blocker “blocks” these receptors so the opposite happens. Propranolol is beta blocker.

2. Clonidine. Clonidine is a sympatholytic medication meaning it blocks the flight or fight response. It’s used to treat high blood pressure but also ADHD and anxiety disorders. Personally, I’ve seen quite a few of these ingestions and they tend to be very unpredictable. The child can be fine one minute and then, with little warning, have a very slow heart rate and be unarouseable.

3. Baclofen: A muscle relaxer.

4. Calcium Channel Blocker. These drugs do what they say– block the flow of calcium from entering heart cells and those that line your blood vessels. Calcium acts to contract things so blocking its flow has the opposite effect. They are used to treat high blood pressure, migraine headaches and Raynaud’s disease. Verapamil would be a drug in this class.

5. Digoxin: I talk extensively about digoxin toxicity in this post.

How do we treat? With the exception of digoxin, there is no specific antidote so it is largely symptomatic support.

1. Give IV fluids. This will help support and raise the blood pressure.

2. Give Calcium. This helps things contract– thereby raising the blood pressure as well.

3. Give a Vasopressor. Vasopressors work to contract blood vessels to raise blood pressure. These would be drugs like dopamine and epinephrine (adrenaline).

There are a few other things to be done but this will give you plenty to write a scene that involves this type of drug ingestion.

Have you written a medical scene that dealt with a drug overdose in your novel?

Deadly Toxin: Mustard Gas


To celebrate Poison’s release, I’m giving away THREE personalized copies of Poison by random drawing to commentors on this weeks posts. To be eligible, you must leave a comment that includes your e-mail address. Must also live in the USA. Drawing will take place midnight on Saturday, February 9th. Winner announced here at Redwood’s February 10th.

I like book titles with double meanings. My first published book was titled, Proof. There were two types of proof the heroine needed. Proof to convict her assailant of his horrific crimes and proof of God in her life.

Poison, the second book in the Bloodline Trilogy, is releasing this month and in this instance—there is an actual nefarious agent (not giving away too much) and a side meaning as well.
What poisons your life? Is it a bad relationship? Is it believing a lie? Is it an actual toxin like dirking too much liquor, using illegal drugs or prescription drugs in ways they weren’t intended?
Writing suspense, particularly with a heavy medical edge, I think requires something unusual to be found. I’m a research hound. I love to learn about new things. And for Poison, I read a lot on different types of toxins.  
Aren’t toxins interesting? How minute substances can make a person ill or end up killing? This is the stuff suspense novels are made from and the lure for every author—finding that one poison—undetectable, fast-acting, easily transmittable or ingested without the victim knowing.
I remember as a youngster hearing the story of how a long-dead great uncle had passed. According to my grandfather, he’d served in the military during WWI and had died as the result of complications from mustard gas exposure.
So lately, in thinking about toxins, I began to wonder what exactly mustard gas was and how did it kill.
Interestingly, I discovered that term “gas” can mean more than just a vaporous substance and can be any chemical substance.
Lethal Gases: Lead to disablement or death.
Harassing agents: Disrupt enemy soldiers.
Accidental Gases: Gases encountered during war that are not related to a chemical agent like excessive gases from gunpowder during a fight.
Mustard gas falls into the first group—lethal gases. Tear gas, for instance, would fall into the second category. 
But how does mustard gas kill?
Mustard gas is also called sulfur mustard and its name is derived from its foggy yellow appearance and mustard like smell. It’s a blistering agent/alkylating agent and comes in many forms: vapor, liquid or solid. When a person comes into contact with the agent, it damages the skin and mucous membranes inside. The chemical liquefies tissue.
Since it freezes at a high temperature, it’s not very effective when it’s cold. It doesn’t spread easily and would fall to the ground before soldiers could be exposed. This property also made it a good weapon because it could stay low on the ground for weeks depending on the temperature and expose unsuspecting troops going into the area. Another factor that made it a good weapon—people adjusted to the smell quickly.
Mustard gas was used first by the Germans in 1917 and was born out of the trench warfare era where new military strategies had to be devised to get men out of their bunkers. The agent was fitted onto artillery shells which were then shot to toward the enemy lines without the accompanying explosion which I’m sure seemed strange to the soldiers at the time.
Hey, why didn’t that thing blow up? What exactly is that yellow fog?
Unfortunately, mustard gas doesn’t often kill expediently. The first symptom was generally red blisters to the skin that developed within 2-24 hours. If the gas was inhaled, these blisters would slowly develop and seal off the airway.
Other symptoms:

  •  Eyes: Irritation, redness, burning, inflammation and even blindness
  • Skin: Itchy redness that is replaced with yellow blister
  • Respiratory system: Runny or bloody nose, sneezing, hoarse throat, shortness of breath, coughing, sinus pain
  • Digestive system: abdominal pain, diarrhea, fever, nausea and vomiting

It was possible for the body to heal if there was a short, brief encounter. Longer, more frequent exposures proved to be more deadly. 
By the end of WWI, chemical agents inured 1 million soldiers and civilians and killed 100,000 people.
Likely, mustard gas wouldn’t be considered favorable to use in chemical warfare these days because of its prolonged activity. 
This link goes to a very powerful article on mustard gas and its effects and was used heavily in the writing of this piece—the italicized areas are from the article. It is definitely worth the read.
What about you? What interesting things have you researched that have ended up in a novel?

Principles of Poisoning: Part 3/3

Today’s post will conclude my three part series on Principles of Poisonings. There’s lots more to talk about in this area so I’m sure I’ll have more on this fascinating topic in the future.

For the last part, I’m going to cover basic treatment guidelines of the poisoned patient. We’re going to assume the patient arrives to the ED alert and breathing.

1. Obtain the patient’s weight. This may seems odd but when we look at whether or not a patient has ingested a toxic amount of the drug it will be determined by the mg/kg of the medicine. For example, if I take 1000mg of acetaminophen, this is a “normal” dose for someone of my weight. And no, I’m not going to tell you my weight. Let’s say, a child weighing 10kg took the same amount. This would be 100mg/kg of drug/body weight ratio. A normal dosing guideline for acetaminophen is 10-15mg/kg so this patient is at 10 times the normal dose.

2. Determine the amount of the drug and the time of ingestion. This can be more challenging than it seems. People don’t usually know the “exact” amount left in a bottle unless it is a medication they take every day. Also, kids are classic for not really being able to say how much they ingested. We assume worst case scenario and go from that point.

3. Call Poison Control. They are the experts. We go over the above information and generally follow their advice. Most often it will be observation and symptomatic support. Remember, patients will also have effects from the drugs we give as well. We want to minimize this if possible and only use these if the patient has an inherent risk of suffering toxic effects that are life threatening. Generally, if the patient presents within one hour of their ingestion to the ED and we are concerned they will have toxic effects, we will give activated charcoal. Syrup of Ipecac is generally out of vogue and no longer used. Then, we’ll obtain a baseline drug level (if it can be measured) and subsequent levels to make sure it is dropping.

Have you experienced a real life overdose/accidental ingestion?

Principles of Poisoning: Part 2/3

What is a nomogram and how does it relate to poisoning? A nomogram is a graph that aids in treatment guidelines for the medical practitioner. Based on the level of drug and the time post ingestion, it basically tells when additional treatment (this would be above and beyond activated charcoal) would be necessary to potentially save the patient’s life.

Here is an example of a nomogram for acetaminophen. When the patient plots in the grey area, we would institute aggressive measures to counteract the effects of the drug… particularly on the liver. Mucomyst is the drug of choice for acetaminophen toxicity.

http://www.merckmanuals.com/professional/print/lexicomp/acetylcysteine.html

Have any of you had experience with acetaminophen toxicity?