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Organophosphate Pesticide Exposure

By Rob Schnepp

You arrive on scene to find a 38-year-old female with a complaint of mild abdominal pain. She states that she has vomited several times, 45 minutes after eating a cheeseburger at a local restaurant. She appears to be very anxious, a little sweaty and obviously uncomfortable; and she graphically describes numerous episodes of watery diarrhea. Her heart rate is 130 beats per minute and her blood pressure is 118/80. She has a runny nose, her pupils are about 2mm 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 the title of this piece had been “Toxic Cheeseburgers: 10 Reasons Why You Should Never Eat Fast Food,” it’s entirely possible that you started thinking about food poisoning. While the signs and symptoms listed above may have lead you down that path, there were other things that should have seemed out of place. Would a patient suffering from food poisoning have pinpoint pupils and wet sounding lungs? Probably not.

I would not expect you to immediately determine an organophosphate exposure, but the point is that a patient of this type may present with mild signs and symptoms. It would then be up to you to make a differential diagnosis and provide the appropriate care. The reality is that this patient may be in serious trouble, and you could be standing at the rare moment when you can intervene at just the right time and truly make a difference.

Since this piece is not about toxic cheeseburgers, let’s get on with the discussion of organophosphates and the concept of proper recognition and the ultimate treatment of an acute exposure. It’s my goal to keep the reading light, informative, and easy to remember. Hopefully, you’ll log off with a better understanding of this group of chemicals, and you can apply it to your own neck of the woods.

At some point in your career, you’ve probably heard about the dreaded class of pesticides called organophosphates. It was most likely from some haz mat guy who said that you could be in real trouble if you were ever exposed to any and that you should take care to protect yourself at all costs. What didn’t get covered, probably, was what to do if you encounter somebody else who’d been exposed. Somebody like the poor guy who works in a bean field somewhere or the farmer who gets exposed to something in his barn that makes him feel all jittery and sick to his stomach. All of a sudden, you find yourself in a position where you wish you’d listened to that haz mat guy a few years ago.

Well, the good news is that you’ve got a second chance! We’ll cover some basics about this group of pesticides and provide you with a few nuggets to file away in case you ever run into this interesting group of chemicals. This is not an article about the chemical makeup of organophosphates per se; it’s more geared at providing medical treatment for the victim of an acute chemical exposure.

With that in mind, let’s look at organophosphates from a broad perspective, specifically their mission in the chemical world. The EPA, for example, looks at pesticides from this perspective: “A pesticide is any substance or mixture of substances intended for preventing, destroying, repelling or mitigating any pest.” This concept alone should let you know that an unintentional exposure could turn out to be a very bad thing. The suffix -cide, in fact, literally means, “to kill.” Pesticides, for example, are designed to kill pests, while rodenticides kill rodents, fungicides kill fungus, and so on and so forth — you get the idea. The thing to keep in mind here is this; pesticides are designed “to kill” pests, but they can be just as effective on humans. That’s what makes this group of chemicals so important: the profound health effects they will have on you or me, or the guy down the street.

Some common organophosphates you may have heard about, or even run into, are malathion, methyl-parathion, diazinon and a host of commercial compounds like 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.

So why are organophosphates so dangerous? First, as stated earlier, they are fairly common, especially in the farming industry, and very effective at doing their job — killing things.

Second, most pesticides are toxic by all routes of entry into the body and have systemic effects. This means that an external exposure to the skin or eyes may cause damage to large-scale body systems like the cardiovascular system or the central nervous system. Damage to these critical body systems, specifically due to organophosphates, could include pinpoint pupils, vomiting, tachycardia and/or bradycardia, seizure-like tremors and respiratory arrest. These substances primarily act on the central nervous system, specifically as a cholinesterase inhibitor.

What this means in laymen’s terms is that an exposure may impair the way our nerves conduct an impulse throughout the body. Imagine for a moment that your body is wired like your house. The brain serves as the main service panel, and the nerves branch out through the body like runs of wiring.  Some go to the kitchen, while others go to the living room and den. When everything works right, the lights go on and off when you flick the switch and all the appliances work like they are supposed to. But what if the wiring arcs, shorts out or becomes compromised? Maybe the lights came on like you expected, 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 that turns off some of the chemical “switches” in your body. In short, a chemical called acetylcholine is secreted by a nerve and travels across a tiny gap to another nerve or an organ that is to be stimulated. Once acetylcholine has completed its mission, the cholinesterase is supposed to break it down and stop the stimulation. This happens a zillion times a day without a problem in a normal, healthy adult; and the whole cycle is completed in a nanosecond. If a person becomes exposed to an organophosphate, however, things change. What happens now is that the acetylcholine does it job, but the specific organophosphate, methyl-parathion, for example, bonds to the cholinesterase and holds it hostage — the cholinesterase can no longer break down the acetylcholine like it’s supposed to. The stimulated cells then go into a sort of hyperdrive and essentially burn themselves up. The manifestations of that excessive stimulation results in a group of symptoms called SLUDGE, which is an acronym for:

  • Salivation
  • Lachrymation (teary eyes)
  • Urination
  • Defecation
  • Gastric disturbance
  • Emesis

The patient may also appear anxious, have muscle tremors, diarrhea, bradycardia or even tachycardia, hypotension and pinpoint pupils. There may also be huge amounts of saliva in the mouth and upper airway, which could ultimately lead to airway compromise. All in all, he is in BIG trouble and the drugs you administer may not even save him. It stands to reason, then, that an acute exposure requires immediate and aggressive therapy; and even then, you may lose the patient.

How do you determine if your patient has been exposed to an organophosphate? A good scene survey perhaps, but more than likely it will the patient presentation and obtaining a good patient history. The part of the story omitted from the beginning of the article was this: The patient 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 you literally need to drag information out of your patients. Usually, if you don’t ask, they don’t tell!

Organophosphate exposures create a unique group of symptoms, and you will need to fit the puzzle together properly in order to see them. Pinpoint pupils are a big clue, so make sure your secondary survey includes a pupil check. The patient may also be wheezing, with 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? The treatment is largely aimed at breaking the hold on cholinesterase. This is not an easy proposition and has to be done with drug therapy. Here again, thorough and safe decontamination must be completed to assure your own safety. Assuming the scene is safe and you have done a good job of decontamination, here are some guidelines:

BLS Actions

  • Protect yourself first!
  • Make every attempt to identify the source of the exposure.
  • Do a good primary and secondary survey.
  • Administer high-flow oxygen. The airway may also require lots of suctioning. Death due to organophosphate exposures is usually from hypoxia 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 patient in a position of comfort — supine may not be the best.
  • Rapid Transport — don’t play doctor on the scene. Once you recognize the situation, get on the road!

ALS Actions (including all the above)

  • Use pulse oximetry if within your scope. Any readings below 93% should indicate respiratory compromise.
  • ECG: Monitor for tachycardia or bradycardia but remember treat the patient, not the monitor. Don’t immediately jump on 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, successful treatment of the underlying problem may correct cardiac disturbances.
  • Large bore IV if applicable. You may be pushing huge amounts of IV fluids and drugs so make sure the line is patent. Take care to use aseptic techniques and ensure that the patient 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 patient with significant inhalation exposures. There may be swelling in the upper airway so intubate early if it is indicated.
  • Administer 2-5 mg’s of atropine IV push or down the ET tube every 2-5 minutes. Your therapy is directed at drying up the secretions. Dilated pupils are an indicator of effectiveness as well as the restoration of an effective heart rate and the diminished effects of the SLUDGE. If administering the atropine via the endotracheal tube, double the IV dose or use high dose atropine diluted in 10 cc’s of saline. This keeps from adding a bunch of fluid to what may already be there. Atropine has no contraindications in this setting. Although it’s not in the scope of practice for most paramedics, the administration of pralidoxime (2-PAM) has been shown to be tremendously effective at treating organophosphate exposures. In regards to the nerve agents (Sarin, Soman, Tabun, etc.), pralidoxime is part of the standard drug therapy to be administered. It can be administered as an infusion at 1 gram over 30 minutes or as a 1 gram bolus. Other studies have shown that an IV infusion of pralidoxime at a rate of 500mg per hour may be effective. This is largely a treatment given in the hospital, but one you should be aware of. The therapeutic goal of either of these drugs is to dry the respiratory secretions and improve the oxygenation of the patient. It’s not unreasonable for a patient to receive more than 500mg’s of atropine in a 24-hour period. This may seem extreme, as we are accustomed to administering atropine in 0.5 and 1 mg doses, but should illustrate the benefit of sustained and aggressive treatment.
  • The patient may also be seizing. If this occurs, treat for seizures per your local protocols.
  • In the event of cardiac arrest, treat it like any other non-chemically induced code.

Other important components to treatment include things not traditionally associated with pre-hospital medicine. In the case of an acute exposure where you suspect organophosphates, 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 patient become stable, it would be helpful to know. It’s also important to understand the need for thorough decontamination and personal protective equipment. The intent of this article is not to discuss the pros and cons of technical decon, but any responder should put this action at the top of the priority list 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 patient yourself.

Additionally, many organophosphate pesticides are mixed in a hydrocarbon media prior to 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 of us in the EMS field use the standard latex rubber gloves for medical calls, but the problem with latex rubber and many hydrocarbons is this: they break down the latex like gasoline in a Styrofoam cup. That’s an extreme example, but your thinking should revolve around making sure you don’t wear any old 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 patient. It’s bad form to show up as a rescuer and end up in the hospital!

Under the best circumstances, chemical exposures are difficult to deal with. We become accustomed to dealing with heart attacks and trauma, but may feel a whole lot less comfortable with the kind of patient described at the beginning of this piece. The keys to being successful in this setting are to remember these 5 basic points:

  • Provide for your own safety first!
  • Try to ID the source of the exposure
  • Decontaminate the patient if it’s your responsibility
  • Provide the appropriate BLS or ALS measures
  • Package the patient 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 patient toward the hospital.

This is where the definitive care takes place. Don’t delay in getting the patient to the most appropriate facility in the shortest amount of time!


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