BY ROB SCHNEPP
You arrive on scene to find a 38-year-old female complaining of mild abdominal pain. She states that she vomited several times, starting 45 minutes after eating a cheeseburger at a local restaurant. She appears to be very anxious, a little sweaty, and graphically describes numerous episodes of watery diarrhea. Her heart rate is 130 beats per minute; her blood pressure is 118/80. She has a runny nose, her pupils are about two millimeters in diameter, and she is oriented but slow to respond to your questions. You listen to her lungs and find them to be “wet-sounding” with a respiratory rate of 32.
Any thoughts on what might be wrong? If this piece had been titled “Toxic Cheeseburgers: 10 Reasons Why You Should Never Eat Fast Food,” you would have thought about food poisoning. Although the signs and symptoms listed above may have led you down that path, other symptoms should seem out of place.
Would a food poisoning victim exhibit pinpoint pupils and wet-sounding lungs? Perhaps not. Although it may be unreasonable to expect you to identify an organophosphate exposure immediately, it should be evident that the victim has a unique combination of signs and symptoms. The reality: This victim may be in serious trouble! If you recognize it, you are right there at just the right time and truly can make a difference.
RECOGNIZING ORGANOPHOSPHATES
Organophospates constitute a group of pesticides designed to kill pests, but they can be just as effective on humans. Keep in mind that the suffix “cide” means “to kill.” Organophosphates comprise just one of the many different categories of pesticides. Some common organophosphates are malathion, methyl-parathion, diazinon, and a host of commercial compounds such as Lorsban and Dursban. It’s interesting to note that the chemical nerve agents Sarin, Soman, and Tabun are also classified as organophosphates-that should give you an idea of how nasty they can be.
Pesticides are dangerous because they are fairly common (especially in agriculture) and very effective at killing pests. Most pesticides are toxic by all routes of entry into the body and could have systemic effects, meaning that an external exposure to the skin or eyes may result in damage to large-scale body systems (e.g., cardiovascular or central nervous systems).
Symptoms of damage to these critical body systems specifically because of or-ganophosphates could include pinpoint pup-ils, vomiting, tachycardia (rapid heart rate of more than 100 beats per minute) and bradycardia (a slow heart rate usually of fewer than 60 beats per minute), seizure-like tremors, and respiratory arrest.
HOW THEY WORK
Organophosphates primarily act on the central nervous system, specifically as a cholinesterase inhibitor, which means an acute overexposure may impair the way a nerve conducts an impulse throughout the body. Imagine that your body is wired like your house. The brain is the main service panel and the nerves branch out through the body like wiring. When everything works right, the lights go on and off when you flick the switch, and all the appliances operate like they are supposed to.
But what if the wiring arcs, shorts out, or is compromised? Maybe the lights came on as you expected or maybe they didn’t. Perhaps they stayed on and couldn’t be turned off no matter what you did. Basically, this is what an organophosphate does. It interferes with the uptake of a chemical compound called cholinesterase, a crucial chemical that turns off some of the chemical switches in your body.
In short, here’s how the chemical transmission part of a nerve impulse occurs. First, a nerve secretes a chemical called acetylcholine, which then travels across a tiny gap to another nerve or to an organ to be stimulated. Once acetylcholine has completed its stimulation mission, another chemical called cholinesterase is secreted that breaks it down and stops the stimulation. This happens a zillion times a day without a problem in a normal healthy adult-the whole cycle is completed in a nanosecond.
If, however, a person is exposed to an organophosphate like methyl-parathion or perhaps a nerve agent, the chemical part of the nerve transmission is compromised. In this case, acetylcholine will still be allowed to do its job, but the specific organophosphate will bond to the cholinesterase and hold it hostage, and the cholinesterase will be unable to break down the acetylcholine as it’s supposed to. The stimulated cells then go into a sort of hyperdrive and essentially burn themselves up.
SYMPTOMS: SLUDGE
The symptoms of excessive stimulation form the acronym SLUDGE:
–Salivation
–Lachrymation (teary eyes)
–Urination
–Defecation
–Gastric disturbance
–Emesis (vomiting)
The SLUDGEing victim may also exhibit anxiety, muscle tremors, diarrhea, bradycardia (or even tachycardia), hypotension (low blood pressure), and pinpoint pupils. There may be huge amounts of saliva in the mouth and upper airway, which could ultimately compromise the airway. All in all, a victim exhibiting such signs could be in BIG trouble, and the drugs that are supposed to counteract the exposure may be ineffective. An acute exposure requires immediate aggressive therapy-even then, you may lose the victim.
DETERMINING EXPOSURE
A good scene survey may provide key indicators of exposure, but more likely the victim presentation and history will tip you off. In the opening scenario, crucial information was omitted. The victim just started a new job with a lawn care service and had spent the entire day applying some “bug killer” that her boss told her to use. She ate the cheeseburger in the car on the way home. Would that have been a good piece of the puzzle to know earlier? Absolutely. But remember, it’s up to you to be the historian in most cases. If you’ve been running EMS calls for any length of time, you know full well that sometimes you have to drag information out of your victims. Usually, if you don’t ask or don’t ask correctly, they don’t tell!
Organophosphate exposures create a unique group of symptoms, especially in the event of a mild overexposure, and you will need to fit the pieces of the puzzle together properly to recognize them. Pinpoint pupils are a big clue, so make sure your secondary survey includes a pupil check. The victim may also be wheezing and have no history of asthma or other respiratory disease. Keep in mind that, in cases of mild overexposure, it may be the subtle things that tip you off.
So, now you have determined that you have an organophosphate poisoning, what next? First, ensure your own safety so you don’t become a victim yourself! If you are an EMT or first responder, focus your efforts on maintaining a good airway-monitoring for any significant changes in blood pressure, heart rate, or level of consciousness-and transport the victim. Advanced level treatments are largely aimed at breaking the hold on cholinesterase. This is not an easy proposition and must be done with drug therapy.
DECONTAMINATION IS ESSENTIAL
For your safety and for the victim’s benefit, perform victim decontamination as early as possible. Decontamination may be accomplished any number of ways, but for the most part, water is the preferred agent of choice. Gross victim decontamination can be as simple as removing any clothing that may be on the affected area and flooding that area with copious amounts of water. Keep track of where the excess water goes, however, since it may spread the contamination to other parts of the victim’s body. Moreover, victims who have not been decontaminated or have been inadequately decontaminated will not be admitted to most hospital emergency rooms. Hospitals get a little touchy about contaminated ERs and will take exception to your showing up at their back door with an improperly decontaminated victim. So, assuming the scene is safe and you have done a good job of decontamination, here are some guidelines.
BASIC LIFE SUPPORT (BLS)
- Protect yourself first!
- Identify the source of the exposure.
- Perform a good primary and secondary survey. Maintaining the airway is critical.
- Administer high-flow oxygen. The airway may also require lots of suctioning. Death from organophosphate exposures is usually because of oxygen deprivation or respiratory failure secondary to neuromuscular failure.
- Obtain a full set of vital signs.
- Determine a baseline respiratory effort and rate, and closely monitor for changes.
- Obtain a baseline mental status, and monitor for changes.
- Put the victim in a comfortable position-the supine position (lying on the back) may not be the best because of vomiting. If the victim is vomiting or if you expect he may do so, place him on his side during transport.
- Rapid transport is essential. Don’t play doctor on the scene. Once you have identified an organophosphate exposure and have performed all actions necessary, get on the road!
ADVANCED LIFE SUPPORT (ALS)
In addition to the above BLS actions, do the following, if possible:
- Use pulse oximetry if within your scope. Any readings below 93 percent indicate respiratory compromise.
- ECG-monitor for tachycardia or bradycardia, but remember to treat the victim, not the monitor. Don’t immediately perform cardiac treatment unless it’s hemodynamically significant. Changes in the heart rate may not respond to traditional cardiotonic drugs. In the case of an organophosphate exposure, successful treatment of the underlying problem (the exposure) may correct the cardiac problems.
- Use a large-bore IV if applicable. You may be pushing huge amounts of IV fluids and drugs, so make sure you have a good, secure, and well flowing IV line. Use aseptic techniques, and ensure that the victim has been fully decontaminated prior to poking holes in his skin.
- Track respirations with a bag valve mask, or intubate if necessary. Watch out for your own lungs when intubating or ventilating a victim with significant inhalation exposures. There may be swelling in the upper airway, so intubate early if it is indicated.
- Administer two to five mgs of atropine through the IV or down the endotracheal tube (or whatever airway adjunct you use) every two to five minutes. If administering the atropine via the endotracheal tube, double the IV dose, or use high-dose atropine diluted in 10 ccs of normal saline. The use of high-dose atropine down the tube eliminates or reduces the possibility of adding a large amount of fluid to what may already be there. Keep in mind that your goal is to dry up the secretions.
- Atropine has no contraindications in this setting.
Pupil dilation indicates treatment effectiveness as does the restoration of an effective heart rate and the diminished effects of SLUDGE.
Although it’s not in the scope of practice for most paramedics, the administration of pralidoxime (2-PAM) may be tremendously effective at treating organophosphate exposures. Regarding the nerve agents (Sarin, Soman, Tabun, etc.), pralidoxime is part of the standard drug therapy. It can be administered as an infusion at one gram over 30 minutes or as a one-gram bolus.
Other studies have shown that an IV infusion of pralidoxime at a rate of 500 mg per hour may be effective. This is largely a treatment given in the hospital, but one of which you should be aware. The therapeutic goal of each of these drugs is to dry the respiratory secretions and improve the victim’s oxygenation. To that end, it may be reasonable for a victim to receive more than 500 mgs of atropine in a 24-hour period. This may seem extreme, since we are accustomed to administering atropine in .5- and 1-mg doses but should illustrate the benefit of sustained and aggressive treatment.
- If the victim is also having seizures, treat for seizures according to your local protocols.
- In the event of cardiac arrest, treat it like any other nonchemically-induced code.
Other important treatment components include actions not traditionally associated with prehospital medicine. In the case of an acute exposure where you suspect organ-ophosphates, make every attempt to identify the offending substance. It’s not as critical if you can’t make a positive ID in the first few minutes, but down the road, should the victim stabilize, it would be helpful to know.
It’s also important to understand the need for thorough decontamination and personal protective equipment. This article does not discuss the pros and cons of technical decon, but any responder should make this action the top priority when dealing with chemical exposures. It’s so important, in fact, that no treatment should begin until you are reasonably sure that you won’t become a victim yourself.
FLAMMABILITY CONCERNS
Additionally, many organophosphate pesticides are mixed in a hydrocarbon (solvent) media before application. This means that if the pesticide is in a liquid form, some sort of flammable liquid could very well be present. It’s not the flammability that should concern you so much, although you should consider the danger, but it’s the effect that most solvents have on latex rubber. Many in the EMS field use the standard latex rubber gloves for medical calls; the problem with latex rubber is that, if exposed to aggressive solvents, it will break down or seriously degrade. The gloves will get slimy or simply just melt away. The reaction is much like pouring gasoline in a styrofoam cup.
That’s an extreme example, but your thinking should revolve around making sure you don’t wear just any pair of gloves and assume you’ll be protected. Each particular substance may have unique incompatibilities with your gloves, so make sure that they will work before putting your hands on an exposed victim. It’s bad form to show up as a rescuer and end up in the hospital!
Five Keys to Success
Under the best circumstances, chemical exposures are difficult to deal with. We become accustomed to dealing with heart attacks and trauma but may not be as comfortable with the medical problems described above. Remember these five keys to success in this situation:
- Provide for your own safety first!
- Identify the source of the exposure.
- Decontaminate the victim if it’s your responsibility.
- Perform the appropriate BLS or ALS measures.
- Package the victim and transport.
The final comment is directed at the single most important governing principle when dealing with chemical exposures: Everything you do should be geared at moving the victim toward the hospital. This is where the definitive care takes place-don’t delay in getting the victim to the most appropriate facility in the shortest time!
ROB SCHNEPP is a career firefighter/paramedic with the Alameda County (CA) Fire Department in the San Francisco Bay Area. He also serves as a hazardous materials specialist with the Region 4 Task Force of the FEMA Urban Search and Rescue team based in Oakland. He is the primary author of Hazardous Materials: Regulations, Response, and Site Operations (Delmar Publishing, Albany, NY, 1998).
