Pesticide poisoning occurs accidentally and intentionally across the world since these products are widely used agriculturally and domestically. Pesticides commonly contain organophosphates, which cause a wide range of symptoms related to muscarinic and nicotinic effects.
Most household and agricultural pesticides are composed of organophosphates and carbamates  . These anticholinesterase compounds are widely available and effective. Hence, accidental and intentional poisoning with these products occurs at a high frequency, particularly in rural regions in developing countries .
Exposure to anticholinesterases may result in acute muscarinic and nicotinic toxicity. Muscarinic signs include diaphoresis, diarrhea, urination, miosis, bradycardia, bronchospasm, bronchorrhea, emesis, excess lacrimation, and salivation (DUMBELS). Meanwhile, nicotinic effects are comprised of muscle fasciculations, weakness, paralysis and possibly cardiovascular consequences such as tachycardia and hypertension .
Other severe manifestations that emerge from pesticide poisoning are mental status changes such as confusion, lethargy, agitation, anxiety, and possibly coma . In cases with delayed toxicity, neuropathy may arise days to weeks post-exposure.
Sequelae such as seizure, loss of consciousness, and respiratory depression may lead to respiratory failure  . Furthermore, other severe outcomes include myocardial infarction, liver and kidney impairment, multisystem failure, and secondary infections . Additionally, cognitive deficits and extrapyramidal signs are considered as potential long-term effects.
The overall clinical presentation is notable for an altered mental status, fasciculations, sweating, and pinpoint pupils. Remarkable findings on an evaluation of the vital signs include hypoxia and dramatic changes in heart rate and blood pressure. Moreover, auscultation of the lungs may reveal wheezing, rhonchi, and distressed breathing while the neurology exam may demonstrate parkinsonian features and possibly paralysis.
Suspicion for organophosphate pesticide toxicity should be high for patients with altered mental status, miosis, excessive diaphoresis, fasciculations and difficulty with respiration. Since this is a clinical diagnosis, the patient's history, exposure risk, and characteristic findings on physical exam are significant components of the workup. Furthermore, assessment of the cholinesterase activity is important for confirmation of the diagnosis.
Organophosphate pesticides act as cholinesterase inhibitors, which explains why the measurement of cholinesterase activity is used as the confirmatory study . Moreover, both red blood cell cholinesterase (RBC AChE) and plasma or pseudo cholinesterase (PChE) can be tested. However, RBC AChE is a more accurate biomarker.
In contrast to time-consuming assays, there is a portable field test known as Test-mate ChE that yields RBC AChE and PChE results within 4 minutes. This has been reported as an effective tool for the measurement of cholinesterase levels in patients with acute organophosphate pesticide poisoning . The use of enzyme assays and confirmation of toxicity is paramount in the monitoring of organophosphates in occupational and military settings .
Administration of atropine reverses or improves the anti-muscarinic manifestations and thereby serves as a diagnostic and therapeutic measure.
Further evaluation is necessary to understand the comprehensive picture. For example, a complete blood count (CBC) exhibits leukocytosis while a complete metabolic panel (CMP) demonstrates hyperglycemia, hypokalemia, hypomagnesemia, increased liver function tests (LFTs) and elevated amylase. Additionally, cardiac enzyme studies may be notable for elevated troponin levels due to myocardial injury . Very importantly, an arterial blood gas is likely to show metabolic and/or respiratory acidosis.