Various symptoms manifest after organophosphate intoxication due to muscarinic, nicotinic, and central nervous system effects. Complications are common, and morbidity occurs due to respiratory center depression, cardiovascular complications, aspiration pneumonia, general weakness, and neurological symptoms. Some studies have reported a statistically significant association between organophosphate intoxication and deep vein thrombosis. However, cases of pulmonary thromboembolism (PTE) resulting from organophosphate poisoning are very rare. A 45-year-old male patient was transferred to our hospital after ingesting an unknown amount of an insecticide and receiving 6 L of gastric lavage at a local hospital. Other than nausea, no symptoms (e.g., dyspnea) were present, but a hemodynamic test showed an elevated lactic acid level, and metabolic acidosis worsened over time. Accordingly, we conducted initial treatment including continuous renal replacement therapy. After 7 hours, the poisoning analysis result was confirmed, and lambda-cyhalothrin and chlorpyrifos (0.441 µg/mL and 0.401 µg/mL, respectively) were detected. We introduced pralidoxime. Although no increase in pseudocholinesterase was found during hospitalization, continuous renal replacement therapy and pralidoxime were discontinued because the patient did not show symptoms of intermediate syndrome, including dyspnea and altered consciousness. The patient complained of abdominal pain on hospital day 8. Abdominal computed tomography was performed to evaluate the possibility of a corrosive injury to the stomach or esophagus, and we confirmed PTE. The D-dimer level was 1.96 mg/L (normal range, 0–0.55 mg/dL). A radiologic examination showed a PTE in the main pulmonary artery leading to the segmental pulmonary artery. After heparinization, the patient was discharged after being prescribed a vitamin K-independent oral anticoagulant. Through this case, we would like to emphasize the need for a thorough evaluation of clinical symptoms because atypical symptoms can occur after poisoning with organophosphate pesticides.
Purpose: Many patients who are acutely poisoned with organophosphorus pesticides have co-ingested alcohol. The purpose of this study was to identify the factors that influence mortality in organophosphate intoxication and the differences between alcohol coingested patients and non-coingested patients, looking at vital signs, length of admission, cholinesterase activity, complications, and mortality. Methods: All patients visiting one Emergency Department (ED) with organophosphate intoxication between January 2000 and December 2012 were reviewed retrospectively. The patients were divided into two groups, alcohol coingested group and non-coingested group. Results: During the study period, 136 patients (alcohol coingested group, 95 patients; non-coingested group, 41 patients) presented to the ED with organophosphate intoxication. Seventy-one alcohol coingested patients (74.1%) vs. 16 non-coingested patients (39.0%) received endotracheal intubation, with results of the analysis showing a clear distinction between the two groups (p=0.001). Twenty-three alcohol coingested patients (24.2%) vs. 1 non-coingested patient (2.4%) required inotropics, indicating a significant gap (p=0.002). Twenty-eight alcohol coingested patients (29.5%) vs. 2 non-coingested patients (4.9%) died, with results of the analysis showing a clear distinction between the two groups (p=0.002). Conclusion: In cases of organophosphate intoxication, alcohol coingested patients tended to receive endotracheal intubation, went into shock, developed central nervous system complications, and more died.
Acute organophosphate intoxication is important because of its high morbidity and mortality. The mortality is still high despite the use of atropine as specific antidotal therapy and oximes for reactivation of acetylcholinesterase. Inhibition of acetylcholinesterase by organophosphate can cause acute parasympathetic system dysfunction, muscle weakness, seizure, coma, and respiratory failure. Acute alteration in conscious state or a coma, which may occur following organophosphate intoxication, is an indication of severe intoxication and poorer prognosis. This acute decline in conscious state often reverses when the cholinergic crisis settles; however, it may be prolonged in some patients. We report on a case of a 60-year-old male who showed prolonged decline in conscious state due to of Central Nervous System (CNS) toxicity after a suicide attempt with organophosphate.
Purpose: The optimal dose of oximes for use in the treatment of organophosphorus pesticide poisoning has not been conclusively established. In this retrospective study, we assessed the effectiveness of the use of high-dose pralidoxime infusion in treating organophosphorus pesticide poisoning. Methods: From January 1998 to December 2009, 71 patients visited the hospital Emergency Department (ED) as a result of organophosphate pesticide intoxication. All of these patients received an initial bolus of 2 g of pralidoxime as the first step of treatment. Patients who then received continuous infusion of pralidoxime at a dose of 500 mg/hr were entered into study group 1 (low dose), and those treated by continuous infusion of pralidoxime at a dose of 1000 mg/hr were entered into study group 2 (high-dose). Plasma cholinesterase activities for each patient were evaluated at ED arrival and re-evaluated 24 hours after pralidoxime infusion. The effectiveness of the two treatment modalities was gauged by comparing the required duration of mechanical ventilation, time spent in the intensive care unit (ICU) and total time spent in the hospital. Results: The mean duration of mechanical ventilation was $9.98{pm}6.47$ days for group 1 and $4.39{pm}6.44$ days for group 2. The respective mean duration of time spent in ICU and the total number of days in the hospital were $16.38{pm}18.84$ days and $21.87{pm}20.16$ days for group 1, and $7.83{pm}9.99$ days and $11.71{pm}13.53$ days for group 2. Highdose pralidoxime treatment was associated with shorter required durations for mechanical ventilation, ICU and hospital stay. In addition, plasma cholinesterase reactivation rates were higher for those patients receiving high-dose pralidoxime treatment. Conclusion: The results suggest that high-dose pralidoxime treatment has greater efficacy for patients suffering from organophosphorus pesticide poisoning.
Purpose: This study investigated the effect on survival rate for organophosphate intoxication patients who received trachostomy. This research was conducted to help identify appropriate treatment of patients who received a trachostomy. Methods: This research was retrospectively conducted using the medical records of 141 patients who arrived at the Chosun University Hospital emergency medical center between Jan 2007 and Dec 2010, suffering from organophosphate intoxication. They were placed in two groups including one which received trachostomy as part of their treatment and one that did not. The effect of each variable on mortality was evaluated by regressionanalysis. Results: Of 141 patients with organophosphate intoxication, 105 of them did not tracheostomy and 16 were dead cohorts (15.2%). Their size of pupil was 1mm. Factors such as amount of organophosphate ingested, PAM time after ingestion, average body temperature, arrival time, atropinization time after ingestion, AST/ALT, Bun/Cr all appeared to be significant factors in death cohorts (P<0.05). 36 patients among the total had tracheostomy and 11 ones of them were in dead cohort (30.6%) and their average age was 58 years. The facts affect the state of patients in dead cohort include the amount of intoxication which between $327.27{pm}194.1ml$, performing intubation 686 mins after intubation, reaching to the hospital after 580mins, injecting PAM 744 mins after intoxication, injecting atropine 627 mins after intoxication. The largest cases of patient's state was found to be stupor with 14 patients (38.9%) the level of Cholinesterase in blood appeared to be significant in dead cohort as $391.00{pm}353.9IU/L$ (P<0.05). Conclusion: Further planned studies are necessary on the use of tracheostomy for treatment of poisoning victims, especially those intoxicated by organophosphorus insecticides.
Purpose: The purpose of this study is to investigate the factors that predict using mechanical ventilation for patients with organophosphate intoxication. Methods: We retrospectively reviewed the medical records of 111 patients with acute organophosphate intoxication and who were treated in our emergency center from January 2000 to December 2008. We compared the toxicologic characteristics, the laboratory findings and the APACHE II scores between the Mechanical Ventilation group (MV group) and the non-Mechanical Ventilation group (the non MV group). Results: Sixty three patients were in the MV group and 48 patients were in the non MV group. In the MV group, the patients had an older age (p<0.001), a larger amount of ingestion (p<0.001), a lower initial serum cholinesterase level (p=0.003), a higher APACHE II score (p<0.001) and they ingested a more toxic agent (p=0.001). There were no significant differences in gender, the type of visit and the arrival time between the MV group and the non MV group. Conclusion: We suggest that the patient's age, the amount of organophosphate ingestion, the toxicity of the agent, the initial serum cholinesterase level and the APACHE II score are important factors to determine if mechanical ventilation will be applied for patients with organophosphate intoxication.
$Basagran^{(R)}$ is a herbicide that is widely used in the field and it acts by interfering with photosynthesis in plants. It consists of bentazone, 2-methyl-4-chlorophenoxyacetic acid (MCPA) and surfactants. Bentazone is commonly used, but poisoning due to Bentazone has not been previously reported in Korea. The patients with toxic effects of bentazone show mild to severe symptoms and various complications. We report here on a case of a woman who intentionally ingested 500 ml of $Basagran^{(R)}$ and she was discharged without complication. As soon as the patient visited the emergency department, we started to treat her as if she had organophosphate intoxication because of the cholinergic symptoms. We could not detect the bentazone in her serum and urine, and we could confirm $Basagran^{(R)}$ ingestion only after getting information from her husband. Bentazone poisoning may induce harmful complications like muscle rigidity, rhabdomyolysis, respiratory failure and cardiac arrest. A detailed history taking, an accurate analysis method and early conservative management will be helpful for patients with acute bentazone poisoning.
A 57-year-old man was transferred to our emergency department with decreased mental status after organophosphate intoxication. He had a four year history of benzodiazepine and hypnotic medication use for chronic insomnia and a depressive mood disorder. He had no previous history of seizures, diabetes mellitus, and hypertension. By hospital day 5, the patient was noted to be awake and to have repetitive jerking movements involving the left upper extremity, and appeared apathetic, depressed and less responsive to external stimuli. A benzodiazepine withdrawal syndrome was subsequently apparent when he developed several generalized tonic clonic seizures and status epilepticus. Using a continuous midazolam intravenous infusion, we successfully controlled the refractory seizure without complications. We present a rare case of status epilepticus from a benzodiazepine withdrawal that developed during the treatment for organophosphate intoxication.
Organophosphate insecticides, commonly used in agriculture, are a gradually increasing cause of accidental and suicidal poisoning. Intoxication can occur by ingestion, inhalation or dermal contact. Exposure to organophosphorus agents causes a sequentially triphasic illness consisting of the cholinergic phase, the intermediate syndrome, and organophosphate-induced delayed polyneuropathy. Acute pancreatitis as a rare complication of organophosphate intoxication has also been infrequently observed. We report a case of intoxication with organophosphate (phos-phamidon) by parenteral exposure (inhalation and/or dermal contact). A 34-year-old male patient was transferred to our Emergency Medical Center and was intubated due to a progressive respiratory failure. He presented with meiotic pupils, cranial nerve palsies, weak respiration, and proximal limb motor weaknesses without sensory changes. He had been employed in filling syringes with phosphamidon during the previous month. Because the patient's history and symptoms suggested organophosphate intoxication with intermediate syndrome, he was mechanically ventilated for 18 days with continuous infusion of atropine and pralidoxime (total amounts of 159 mg and 216 g, respectively). During his admission, hyperamylasemia and hyperli-pasemia were detected, and his abdominal CT scan showed a finding compatible with acute pancreatitis. He was administered a conservative treatment with NPO and nasogastric drainage. The patient was discharged and showed neither gastrointestinal nor neurologic sequelae upon follow up at one week and three months.