Journal of Clinical Toxicology
Open Access
ISSN: 2161-0495
+44 1478 350008
ISSN: 2161-0495
+44 1478 350008
Case Report - (2024)Volume 14, Issue 2
Organophosphates are chemicals used in pesticides. These compounds are acetylcholinesterase inhibitors and prevent the breakdown of acetylcholine. The accumulation of acetylcholine leads to the activation of muscarinic receptors and the creation of cholinergic effects, including increased secretions. It also causes overstimulation of nicotinic receptors, which can lead to respiratory arrest, which is the most common cause of death in organophosphate poisoning. Drug treatment is with atropine and enzyme activator such as pralidoxime. In this study, we presented a 40-year-old man who presented to the emergency room due to suicide with organophosphate poisoning, who was successfully treated with a combination of atropine and magnesium sulfate instead of pralidoxime.
Organophosphates; Poisoning; Magnesium sulphate; Nicotinic; Symptoms; Atropine
Organophosphates (OPs) are one of the main insecticides that have been used since the mid-1940s. Due to the phosphorylation of acetylcholinesterase and its inhibition, this substance leads to an increase in the persistence of acetylcholine in nerve synapses and cholinergic toxicity [1]. Symptoms are usually divided into three groups: Muscarinic, nicotinic and central symptoms. Diagnosis is based on clinical signs and symptoms, as well as measurement of inhibition of acetylcholinesterase activity of red blood cells and inhibition of plasma acetylcholinesterase activity [2]. Treatment is generally done by prescribing atropine and enzyme activators such as pralidoxime. Poisoning with organophosphorus is common in many developing countries, especially in countries where there are many agricultural processes, either accidentally or intentionally [3]. Examining the clinical symptoms after this poisoning and various treatment methods to prevent its morbidity and mortality will be of great importance. In this study, we present a 40-year-old patient who was referred to the emergency room with organophosphorus poisoning and cholinergic symptoms and was successfully treated with a combination of atropine and magnesium sulfate.
A 40-year-old male patient referred to the emergency department of the poisoning department of Imam Reza Hospital in Mashhad after deliberately consuming 100 ml of organophosphorus poison with the intention of committing suicide with cholinergic symptoms. At the time of visit, the patient was fully conscious and had acute cholinergic symptoms such as dizziness, anxiety, pallor, tremors, sweating, sialorrhea, tears, decreased heart rate, and decreased breathing rate. The patient's vital signs included blood pressure of 105/70 mmHg, heart rate of 65, breathing rate of 10 times per minute, oxygen saturation percentage of 96%, and body temperature of 37.3 °C. The patient was treated with oxygen therapy, serum therapy, and atropine until the symptoms were resolved and the necessary tests were sent, including measuring the amount of acetylcholinesterase enzyme in red blood cells and serum. Due to the severity of the patient's symptoms and severe respiratory distress, the patient was intubated and subjected to mechanical ventilation with a ventilator and was admitted to the ICU. After 72 hours, according to the improvement of vital signs and the patient's consciousness, he was extubated and according to the continuation of cholinergic symptoms in the patient, the administration of atropine was continued. During the examination, the patient complained of severe muscle weakness, so that the muscle strength of the upper limbs was estimated to be one-fifth and lower limbs was two-fifths. According to the unavailability of pralidoxime and previous studies on the effectiveness of magnesium sulfate, 2 grams of intravenous magnesium sulfate was prescribed to the patient daily. In order to prevent the possible side effects of magnesium sulfate, the patient's vital signs, electrocardiogram and deep reflexes were repeatedly checked and no pathological findings were found. Para-clinical examination including complete blood cell count, urea, creatinine, coagulation factors and venous blood gasometry were reported within normal range. The level of acetylcholinesterase enzyme in the patient's serum and red blood cells at the first check-up was evaluated 517 U/L (normal range 4620-11500) and 0.6 IU/ml (normal range more than 4.2) respectively. In the course of hospitalization and treatment, the amount of these enzymes increased and reached the normal range. The patient was discharged after 10 days with a good general condition and no special complications. Our study in this case report showed that magnesium sulfate is effective in reducing nicotine symptoms and especially in improving proximal muscle weakness. However, there is a need for more studies to determine the effective dose used, the starting time of the drug and the prevention of its possible side effects.
Organophosphates are chemical agents that are used as insecticides, fungicides and herbicides worldwide for pest control. Studies have shown that exposure to these substances can affect the nervous system and cause Parkinson's disease and other neurological disorders [4]. Also, by affecting the reproductive system, they cause infertility and birth defects of the fetus. Respiratory diseases, endocrine disorders, skin problems and leukemia have also been reported for these substances. These side effects can be different depending on the type of substance and dosage. Poisoning with organophosphates occurs due to occupational, accidental or intentional reasons [3]. Intentional consumption of these substances is one of the most important causes of death in developing countries due to their easy access and the lack of a monitoring system for control, and it can be said that one third of suicides in the world are due to the intentional consumption of pesticides it happens. Organophosphates are absorbed through the skin, digestive tract, conjunctiva and lungs and deactivate acetylcholinesterase by phosphorylating the serine hydroxyl group in the active site of the enzyme. The main role of acetylcholinesterase is to terminate signaling at cholinergic synapses by breaking down the neurotransmitter acetylcholine into choline and acetic acid [5]. Acetylcholinesterase is present in the central nervous system, peripheral nervous system, neuromuscular junction and red blood cells. Now, if it is inhibited by organophosphates, it causes the accumulation of acetylcholine in the synapses, and as a result, it causes excessive stimulation of acetylcholine receptors (Table 1).
| Aspect | Description |
|---|---|
| Chemical nature | Organophosphates are chemicals used in pesticides. |
| Mechanism of action | They are acetylcholinesterase inhibitors, preventing the breakdown of acetylcholine. |
| Physiological effects | Activation of muscarinic receptors causing cholinergic effects such as increased secretions. |
| Overstimulation of nicotinic receptors, potentially leading to respiratory arrest. | |
| Treatment | Atropine: To counteract cholinergic effects by blocking muscarinic receptors. |
| Enzyme activator (e.g., pralidoxime): To reactivate acetylcholinesterase. | |
| However, in this study, a 40-year-old man with organophosphate poisoning was successfully treated. | |
| Atropine-to manage cholinergic effects. | |
| Magnesium sulfate-used instead of pralidoxime. | |
| Case presentation | A 40-year-old man presented to the emergency room due to suicide with organophosphate poisoning. |
| Successful treatment involved a combination of atropine and magnesium sulfate. | |
| Outcome | The patient responded well to the treatment and survived the poisoning incident. |
Table 1: This table provides a concise overview of organophosphates, their effects, standard treatment, and a specific case where the treatment protocol was modified with successful outcomes.
Acetylcholine receptors are central, muscarinic, and nicotinic, and their excessive stimulation causes side effects such as dizziness, anxiety, restlessness, headache, tremors, confusion, convulsions, decreased breathing, rhinorrhea, sweating, salivation, diarrhea, and frequent urination, bradycardia, tachycardia and high blood pressure will follow [2]. The initial treatment includes removing the patient's clothes and decontamination of the skin by washing. In case of ingestion of organophosphorus, gastric lavage with activated charcoal is performed when no more than 2 hours have passed after consuming the poison. Support measures including maintenance of ventilation, cardiovascular monitoring are also performed. Atropine is used in drug treatment with the aim of reducing the stimulation of muscarinic receptors that are affected by the accumulation of acetylcholine, which leads to a decrease in the secretion of saliva, tears, nausea, vomiting, diarrhea, controlling bradycardia and reducing bronchial secretions [6]. Also, its effect on CNS is limited due to its low fat solubility. Despite numerous attempts to synthesize newer oximes, currently only four oximes (pralidoxime, obidoxime, trimedoxime, HI-6 oxime) are used for therapy. These different oximes can activate cholinesterase inhibited by different organophosphorus compounds in different ways [7,8]. Pralidoxime is the most common oxime worldwide that is used as an antidote for organophosphates [9]. The recommended dose of pralidoxime according to the WHO guidelines is initially as a bolus of 30 mg/kg followed by an infusion of 8 mg/kg per hour until clinical improvement occurs [10]. Several clinical studies have shown its beneficial effects in reactivating acetylcholinesterase in red blood cells. They have also emphasized that administration of oximes within 24 hours after poisoning is necessary for effectiveness. Therefore, oxime should be prescribed as soon as organophosphorus poisoning is diagnosed. However, there are conflicting results regarding the use of oximes. The effectiveness of oximes can vary depending on the type of organophosphorus, the amount of organophosphorus, the time of oxime administration and its inappropriate dose [9]. Recent studies have found the simultaneous use of two drugs, edrophonium and oximes, to be effective in restoring and modulating the activity of the acetylcholinesterase enzyme and reducing the symptoms caused by the accumulation of acetylcholine [11]. Also, another study has reported hydroxamic acid to be effective in reactivating acetylcholinesterase inhibited by organophosphorus compounds [12]. The effect of oximes is limited by high concentration of organophosphorus because high concentration of toxin can reinhibit the enzyme activated by oxime. Currently, there is no type of oxime that can act against all types of organophosphate pesticides and their side effects [13]. Also, the effectiveness of this substance has been reported in two small studies on humans [14]. Thus, intravenous injection of 4 grams of magnesium sulfate led to an improvement in neuromuscular function and a decrease in mortality. However, since the number of people studied was small and non-randomly selected, the dosage of magnesium sulfate and other aspects of the use of this drug were not evaluated; more evaluation should be done for the accuracy of these results. Also, in this study, the effectiveness of oximes (pralidoxime) on reducing the complications of organophosphorus poisoning was not confirmed [15]. In a study by Kiss, et al. [16], intravenous magnesium sulfate resulted in the disappearance of ventricular premature contractions. It was also stated that magnesium inhibits the direct effect of organophosphates on the sodium potassium ATPase pump and thus prevents the release of acetylcholine into the synaptic space [16-18]. In another study, Singh, et al. [19], administered 4 grams of magnesium sulfate intravenously to patients poisoned with organophosphorus and observed that neuro-electrophysiological deficits improved [18,19]. In Bilalimode's study, administration of intravenous magnesium sulfate led to a reduction in the duration of hospitalization and improvement of symptoms in patients suffering from organophosphorus poisoning [20]. Finally, it was reported that the use of magnesium sulfate in organophosphate poisoning reduced treatment costs, length of hospital stay and mortality compared to those who did not receive magnesium sulfate [21]. In 2013, Basher, et al. [22], investigated the effect of magnesium sulfate on the toxicity of organophosphate pesticides, and no adverse effects of magnesium were reported. In our study, no side effects were observed in patients receiving magnesium sulfate [22]. In a study, the role of fresh plasma and magnesium sulfate in the treatment of acute toxicity of organophosphamide insecticides was investigated and the results showed that adding magnesium sulfate and fresh plasma to patients poisoned with organophosphorus reduces the acute toxicity of organophosphamide and reduces the length of hospitalization and mortality. The results of this study were consistent with our findings. Magnesium sulfate is also used to control tachycardia, ventricular arrhythmias and muscle fasciculation’s, which is why it is preferred over traditional treatments [21].
In our study, due to the unavailability of pralidoxime, amount of 2 grams intravenous magnesium sulfate was used and its favorable effects in increasing muscle force were revealed in the patient after 24 hours. The results of various studies show that the timely diagnosis and management of this poisoning provide a favorable prognosis for the patient but if care is not taken, it can lead to a progressive clinical course. As mentioned before, atropine and oximes are antidotes of organophosphates. However, in recent years, research on new adjuvant treatments and inexpensive drugs such as sodium bicarbonate, magnesium sulfate and antioxidants has expanded.
The authors declare no conflicts of interest.
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Citation: Hakemi A (2024) A Case of 40-Year Old Man with Organophosphate Poisoning that his Nicotinic Symptoms Responded Dramatically to Magnesium Sulphate. J Clin Toxicol. 14:559.
Received: 27-Feb-2024, Manuscript No. JCT-24-29825; Editor assigned: 29-Feb-2024, Pre QC No. JCT-24-29825 (PQ); Reviewed: 14-Mar-2024, QC No. JCT-24-29285; Revised: 21-Mar-2024, Manuscript No. JCT-24-29285 (R); Published: 28-Mar-2024 , DOI: 10.35248/2161-0495.24.14.559
Copyright: © 2024 Hakemi A. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.