Pesticides - Clinical Tree

Essentials

1
Acute pesticide poisoning is an important cause of morbidity and mortality worldwide, in particular in the Asia-Pacific region.
2
Existing systems for classifying the toxicity of pesticides are imperfect, whereby the toxicity of even ‘slightly hazardous’ pesticides is sometimes significant. Moderate-to-highly toxic pesticides may have a case-fatality rate of between 5% and 70% in patients with self-poisoning.
3
In addition to the pesticide constituent, other components of the formulation can also contribute to its toxicity. For example, concentrated formulations, or certain salts, solvents or surfactants can lead to worse outcomes. So, different formulations of the same pesticide component can have differing toxicity.
4
Diagnosis is based on a history of exposure and clinical features. In the absence of a history, a high index of suspicion for pesticide poisoning is required.
5
Many pesticides have a delayed onset of clinical manifestations. All patients with oral exposure should be monitored for a minimum of 6 to 48 hours post-ingestion depending on the pesticide involved.
6
Resuscitation and supportive care are priorities in managing acute pesticide poisoning. Patients manifesting significant poisoning require prolonged admission, preferably in an intensive care unit.
7
The risk of secondary contamination to health care workers is low when universal precautions are used.
8
The specific antidote for anticholinesterase pesticide poisoning (organophosphates [OPs], carbamates) is atropine, which should be administered as soon as possible and titrated to effect. Data supporting the efficacy of pralidoxime have been used for acute OP poisoning but data supporting its efficacy are limited, and some studies have suggested harm.

Introduction

Pesticide self-poisonings account for 30% of completed suicides globally. As with pharmaceutical poisoning, the toxicity of pesticides varies between individual compounds. In general, however, pesticides are intrinsically more toxic than pharmaceuticals, although not all pesticide exposures lead to clinically significant poisoning. In Australia, most acute pesticide exposures are accidental and the majority of patients do not require admission to hospital.

Pesticide poisoning can occur due to either acute (intentional self-poisoning) or chronic (such as occupational) exposures. Acute poisoning is of more importance to the emergency physician and is the focus of this chapter.

A pesticide is any chemical used for the control of a plant or animal, and these products encompass hundreds of chemicals. They can be sub-classified in terms of their intended target, the most common being insecticides, herbicides (selective or non-selective, see chapter 25.16 ), fungicides, rodenticides and nematocides. Other methods for classification that have been used include toxicity to animal species (LD ₅₀ ; dose that kills 50% of animal subjects), mechanism of action and chemical structure.

An accurate risk assessment is necessary in each patient with acute pesticide poisoning (see Chapter 25.1 ).

Owing to the low incidence of pesticide poisoning, clinicians do not always consider it in the differential diagnosis. Case reports from Australia describe delays in the diagnosis of pesticide poisoning because this possibility was not considered initially.

This chapter focuses on agricultural chemicals used in Australasia, in particular insecticides (OPs and carbamates) Table 25.15.3 summarises the clinical manifestations and management of selected pesticides.

Aetiology and pathophysiology

Acute intentional self-poisoning with pesticides commonly requires admission to hospital and ongoing care. However, significant poisoning may also occur with accidental (e.g. storage of a pesticide in a milk carton) or criminal exposures.

The pathophysiology of acute pesticide poisoning and therefore its clinical manifestations vary widely between individual compounds, see Table 25.15.3 . Many pesticides induce multisystem toxicity due to interactions with a number of physiological systems. The mechanisms of toxicity in humans frequently bear little relation to that in the target pest. Frequently such mechanisms are poorly described; therefore less information is available to guide the management of these exposures.

It should be noted that proprietary pesticide products contain co-formulants, in particular hydrocarbon-based solvents. Herbicide products also contain surfactants to enhance herbicide penetration into the plant. These co-formulants can contribute to the toxicity of a pesticide product and in some cases are more toxic than the active pesiticide constituent.

Epidemiology

Acute pesticide poisoning is a major issue in developing countries of the Asia-Pacific region, and OPs are considered the most important cause of death from acute poisoning worldwide. In developed countries, however, the incidence of severe pesticide poisoning is relatively low. Nevertheless, it may be higher in rural areas because of greater access to concentrated formulations.

Prevention

Primary exposures

Regulatory restrictions to the availability of highly toxic pesticides may contribute to a decrease in mortality from self-poisoning. In Australia, for example, highly toxic pesticides such as paraquat, organochlorines and parathion are heavily regulated, so poisonings are increasingly rare. The proper storage, handling and use of pesticides can prevent accidental exposures and associated health consequences.

Secondary exposures or nosocomial poisoning

Secondary exposure refers to staff and family members being exposed to poisoned patients, predisposing them to nosocomial poisoning. These are exceptionally rare and occur in the setting of staff who are not taking universal precautions and not using decontamination (e.g. of the skin) if exposed to such an agent, usually via bodily fluids. Although mild symptoms—such as nausea, dizziness, weakness and headache—have been reported, these resolve after exposure to fresh air and are likely due to inhalation of the hydrocarbon solvent. Universal precautions including nitrile gloves are most likely to provide sufficient protection for staff members. Dermal decontamination is performed by washing spilt pesticide off the patient with soap and water while removing and discarding contaminated clothes. Staff with dermal exposure to a poisoned patient’s bodily fluids should wash their skin with soap and water as soon as practicable.

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