Purpose: Nutritional therapy is a crucial component of therapy for critically ill patients, but there is a lack of nutritional support guidelines for organophosphate (OP) poisoning, likely due to the gastrointestinal effects of atropine, the main antidote for OP. This study investigated whether enteral nutrition (EN) during atropinization is acceptable for mechanically ventilated patients after OP poisoning.
Methods This retrospective study classified 82 patients with OP poisoning according to whether they were fed during atropinization while on mechanical ventilation (MV). Data on the baseline characteristics, nutritional support, and clinical outcomes were compared. Univariate and multivariate regression models were constructed to analyze the associations between atropine administration for OP poisoning and feeding intolerance-related EN after adjustment for risk factors.
Results Eighty-two patients received EN after 72 hours on MV, and 40 of them simultaneously received 2 mg/hr atropine for the first 120 hours after EN initiation. The overall incidence of feeding intolerance was 57.3% during the first 12 days after EN initiation and did not differ according to atropine administration. Appropriate atropinization during EN in regression model 1 and the dosage of atropine administered during EN and the duration of EN during atropinization in model 2 were not associated with feeding intolerance in patients on MV after OP poisoning.
Conclusion Appropriate atropinization is not associated with feeding intolerance after EN provision in patients on MV after OP poisoning. This study will help establish nutritional guidelines for OP poisoning patients. More research on nutritional support is needed to validate our results.
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.
In this study, we report the case of a 59-year-old male patient with organophosphate pesticide poisoning. He visited the local emergency medical center after ingesting 250 ml of organophosphate pesticide. The patient's symptoms improved after the initial intravenous infusion of pralidoxime 5 g and atropine 0.5 mg. However, 18 hours after admission, there was a worsening of the symptoms. A high dose of atropine was administered to improve muscarinic symptoms. A total dose of 5091.4 mg of atropine was used for 30 days, and fever and paralytic ileus appeared as side effects of atropine. Anticholinergic symptoms disappeared only after reducing the atropine dose, and the patient was discharged on the 35th day without any neurologic complications.
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Pneumatosis cystoides intestinalis and portomesenteric venous gas are uncommon radiological findings, but are found commonly in cases of bowel ischemia, or as a result of various non-ischemic conditions. A 72-year-old man visited an emergency center with altered mental status 2 hours after ingestion of an unknown pesticide. On physical examination, he showed the characteristic hydrocarbon or garlic-like odor, miotic pupils with no response to light, rhinorrhea, shallow respiration, bronchorrhea, and sweating over his face, chest and abdomen. Laboratory results revealed decreased serum cholinesterase, as well as elevated amylase and lipase level. We made the clinical diagnosis of organophosphate poisoning in this patient based on the clinical features, duration of symptoms and signs, and level of serum cholinesterase. Activated charcoal, fluid, and antidotes were administered after gastric lavage. A computerized tomography scan of the abdomen with intravenous contrast showed acute pancreatitis, poor enhancement of the small bowel, pneumatosis cystoides intestinalis, portomesenteric venous gas and ascites. Emergent laparotomy could not be performed because of his poor physical condition and refusal of treatment by his family. The possible mechanisms were believed to be direct intestinal mucosal damage by pancreatic enzymes and secondary mucosal disruption due to bowel ischemia caused by shock and the use of inotropics. Physicians should be warned about the possibility of pneumatosis cystoides intestinalis and portomesenteric venous gas as a complication of pancreatitis following anticholinesterase poisoning.
Purpose: Despite the clinical and socio-economic impact of acute poisoned patients, many of the treatments are not standardized in Korea. Moreover, no formal training that is specifically focused on clinical toxicology exists. Rather, training and education are conducted case by case in various institutions. This study was conducted to develop a standardized simulation-based clinical toxicology training curriculum for healthcare providers. This program will focus on specific assessment and treatment of critical toxicology patients, specifically those who have been poisoned with organophosphate. Methods: The study was performed using a pre- and post-design to determine the effects of implementation of this program. The study was conducted at eight different urban teaching hospitals in a simulated room in the clinical area. The study was targeted to 19 groups composed of emergency residents and nurses. Simulation-based learning was conducted for each group. Results: All 19 groups achieved the minimum passing score of 75%. Implementation of the program led to improved performance rates for overall management and cooperative moods competency (p<0.01). Inter-rater agreement between the two evaluators was excellent. In general, the participants thought the program was realistic and were able to recognize and improve the competencies needed to care for organophosphate poisoned patients. Conclusion: Simulation-based learning is an effective educational strategy that can be applied to improving and understanding proper care for rare but critical patients. This program was effective at improving team performance and cooperative moods when managing an organophosphate poisoned patient in the Emergency Department.
Purpose: Cardiac complications may occur in cases of organophosphate (OP) poisoning. However, a few studies regarding patterns of cardiac toxicity as determined by transthoracic echocardiography (TTE) after exposure to OP have been reported. In the current study, the authors examined cardiac functions using TTE in patients with myocardial injury caused by exposure to OP. Methods: A retrospective review was conducted on 16 consecutive cases of OP poisoning with myocardial injury (defined as elevated troponin I within 48 hours of arrival at the regional emergency center in South Korea and diagnosed and treated at the center from January 2012 to November 2014. Results: TTE was performed in 11 (69%) of the 16 patients with an elevated troponin I (TnI) level within 48 hours. Of these 11 patients, 5 patients (45.5%) exhibited reduced ejection fraction (EF), and 3 exhibited regional wall motion abnormality (RWMA). Two patients (18.2%) had both reduced systolic function and RWMA. Two of the 5 patients with reduced EF returned to normal systolic function, however two patients did not regain normal systolic function after admission. One patient expired due to multiple organ failure, and 4 patients were transferred with a moribund status. Twelve of 15 patients who survived to discharge (at 4 to 35 months) were followed. Five of these patients died during follow-up and 7 survived without further complications. Conclusion: OP can cause reversible cardiac dysfunction including reduced systolic function and RWMA. Serum TnI may be useful for initial assessment of cardiac function during the workup of patients suffering from OP poisoning. After the initial assessment of cardiac enzyme, further evaluation with TTE in patients with abnormal cardiac enzyme will be necessary to understand the cardiac toxicity.
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.
Purpose: Carbamate insecticides are potent cholinesterase inhibitors capable of causing severe cholinergic toxicity. Use of carbamate rather than organophosphate insecticides has been increasing. Compared with organophosphate poisoning, relatively few studies have investigated carbamate-associated acute pancreatitis. We investigated general characteristics and pancreatitis of carbamate poisoning and the predictors, among those readily assessed in the emergency department. Methods: We performed a retrospective review of consecutive patients, aged over 18 years, who were admitted between January 2008 and April 2012 to an emergency department (ED) of an academic tertiary care center for treatment of carbamate poisoning. Patients who exhibited poisoning by any other material, except alcohol, were excluded. After application of exclusion criteria, patients were divided according to carbamate-induced pancreatitis and non-pancreatitis groups. Results: A total of 41 patients were included in this study. Among these 41 patients, the prevalence of acute pancreatitis was 36.6% (15 patients). Initial blood chemistry tests showed a statistically higher glucose level in the pancreatitis group, compared with the non-pancreatitis group (222, IQR 189-284 vs. 137, IQR 122-175 mg/dL, P<0.05). Regarding clinical courses and outcomes, a significantly higher proportion of patients developed pneumonia [10 (66.7%) vs. 6 (23.1%), P<0.05] and had a longer hospital stay (7 days, IQR 6-12 vs. 5 days, IQR 2-11, P<0.05), but no difference in mortality, in the pancreatitis group vs. the non-pancreatitis group. In multivariate analysis, the initial glucose was showing significant association with the presentation of carbamate-induced acute pancreatitis (odds ratio 1.018, 95% confidence interval 1.001-1.035, P<0.05). Conclusion: Carbamate-induced acute pancreatitis is common, but not fatal. Initial serum glucose level is associated with acute pancreatitis.
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: Organophosphate insecticide poisoning is common in Korea, but there is no definitive guideline for determining the severity of the poisoning and the predictive factors. Therefore, we evaluated the organophosphate poisoned patients and we divided them into two groups, the survivors and the dead, and the results might be useful for treating organophosphate poisoning patients. Methods: We performed a retrospective analysis of 68 organophosphate poisoned patients who visited the Chosun University Hospital Emergency Medical Center during a 24-month period from January, 2007 to December, 2008. We made a work sheet of the patients' characteristics and the collected data was analyzed and we compared this data between the survivor group and the dead patient group. Results: There were significant differences between the survivor group and the dead patient group for the mean age, the alcohol intake state and the typically expressed signs. The dead patients had lower blood pressure, tachycardia and a lower Glasgo Coma Score (GCS) score than the survivor group. On the arterial blood gas analysis, the dead patients had more severe acidemia and they had lower saturations. Increased serum amylase levels were found in the dead patients. The survivors'initial and follow up serum pseudocholinesterase activity (after 6~8 days) was significantly higher than that of the dead group. The total amount of atropine injected to patient was less in the survivors than that in the dead patients. Conclusion: Old age and expressing the typical intoxication signs, a lower GCS score and blood pressure, showing acidosis on the gas analysis and low serum cholinesterase activity may be useful as poor prognostic indicators for patients with organophosphate poisoning. We suggest that physicians must pay careful attention to the signs and prognostic factors of organophosphate insecticide poisoned patients.
Purpose: Various electrocardiogram (ECG) changes can occur in patients with acute organophosphate poisoning (OPP) and may be associated with the clinical severity of poisoning. The present study aimed to evaluate the extent and frequency of ECG changes and cardiac manifestations, and their association with acute OPP clinical severity. Methods: Seventy-two adult patients admitted to our emergency department with a diagnosis of acute OPP were studied retrospectively. ECG changes and cardiac manifestations at admission were evaluated. ECG changes between respiratory failure (RF) group and no respiratory failure (no RF) groups were compared. Results: Prolongation of QTc interval (n=40, 55.6%) was the most common ECG change, followed by sinus tachycardia (n=36, 50.0%). ST-T wave changes such as ST segment elevation or depression and T wave change (inversion or non-specific change) were evident in 16 patients (22.2%). Prolongation of QTc interval was significantly higher in the RF group compared with the no RF group (p=0.03), but was not an independent predictor for RF in acute OPP (OR; 4.00, 95% CI; 0.70-23.12, p=0.12). Conclusion: While patients with acute OPP can display ECG changes that include prolongation of QTc interval, sinus tachycardia, and ST-T wave changes at admission, these changes are not predictors of respiratory failure.
Purpose: Acute organophosphate (OP) poisoning may be monitored by measuring the acetylcholinesterase (AChE). It is important to assess severity and establish prognostic tests in the early stage of OP poisoning. The aim of this study was to look at the relationship between various clinical aspects of the OP poisoning, prognostic indicators of OP poisoning including Simplified Acute Physiology Score (SAPS) 3, and the associated changes in AChE levels. Methods: Clinical data and initial AChE levels from thirty-seven patients with OP poisoning were prospectively reviewed from 12 teaching hospitals in South Korea from August 2005 to July 2006. Clinical manifestations at the time of arrival such as miosis, respiratory abnormality, salivation, urinary incontinence, GCS score, AVPU scale, need for intubation, and mechanical ventilation requirements were recorded. SAPS 3 was calculated using clinical data and laboratory results. Results: The median level of AChE was 9.8 (1.3-53.6) U/gHb. There was no significant difference in AChE levels between the groups with and without cholinergic symptoms. The median level of AChE of the patients who required intubation and those who did not were 3.5 U/gHb and it 19.7 U/gHb respectively (Mann-Whitney test; p<0.001). The AChE levels were also significantly different (p=0.007) in patients who needed mechanical ventilation compared to those who did not with AChE levels found to be 3.1 U/gHb and it was 14.8 U/gHb, respectively. Level of consciousness assessed using the AVPU scale was correlated with AChE levels (Kruskal-Wallis test; p=0.013). GCS score were correlated with AChE levels (p=0.007, Spearman's rho = 0.454). In addition, the lower the level of initial AChE, the longer the ICU stay (p=0.029, Spearman's rho=-0.380). SAPS 3 was inversely correlated with the initial AChE (p<0.001, Spearman's rho=-0.633). Conclusion: In the acute OP poisoning, low AChE levels appear to help indicate the severity of poisoning. The initial AChE level may be a useful prognostic parameter for acute OP poisoning.
Purpose: The major complication of acute organophosphate (OP) poisoning is respiratory failure as a result of cholinergic toxicity. Many clinicians find it difficult to predict the optimal time to initiate mechanical ventilation (MV) weaning, and as a result have tended to provide a prolonged ventilator support period. The purpose of this study is to determine any clinical predictors based on patients characteristics and laboratory findings to assist in the optimal timing of mechanical ventilator weaning. Methods: We reviewed medical and intensive care records of 44 patients with acute OP poisoning who required mechanical ventilation admitted to medical intensive care unit between July 1998 and June 2007. Patient information regarding the poisoning, clinical data and demographic features, APACHE II score, laboratory data, and serial cholinesterase (chE) levels were collected. Base on the time period of MV, the patients were divided into two groups: early group (wean time < 7 days, n = 28) and delayed group (${geq}$ 7 days, n = 16). Patients were assessed for any clinical characteristics and predictors associated with the MV weaning period. Results: During the study period, 44 patients were enrolled in this study. We obtained the sensitivity and specificity values of predictors in the late weaning group. APACHE II score and a reciprocal convert of hypoxic index but specificity (83.8%) is only APACHE II score. Also, the chE concentration (rho = -0.517, p = 0.026) and APACHE II score (rho = 0.827, p < 0.001) correlated with a longer mechanical ventilation duration. Conclusion: In patients with acute OP poisoning who required mechanical ventilation, the APACHE II scoring system on a point scale of less than 17 and decrements in cholinesterase levels on 1-3 days were good predictors of delayed MV weaning.
Purpose: Owing to organophosphate-pyrethroid mixtures are widely used, suicidal or unintentional poisoning is common. But there have been relatively few reports of poisoning. The purpose of this study is to evaluate the difference of the severity and toxicity between organophosphate-pyrethroid mixtures poisoning and single organophosphate poisoning. Methods: From August 2005 to July 2006, 65 patients presented with organophosphate-pyrethroid mixtures poisoning to emergency medical center. Date were gathered by report form it was drawn up. Results: 65 patients were enrolled in 28 hospitals and their mean age was $56.5{pm}16.2$ years old. The most common cause of poisoning was suicide, in 52 cases(80%). Chlorpyrifos-cypermethrin, malathion-esfenvalerate were the most frequent chemicals involved, and the mean ingestion amount was 135.4ml. The most common symptom of the patients was nausea/vomiting, in 16 patients. The average GCS score was 13. The mean ICU stay was $4.4{pm}5.2$ days, and mortality was 3.1%. Conclusion: The severity and toxicity of organophosphate-pyrethroid mixture poisoning were lower than that of single organophosphate poisoning.
Purpose: Organophosphorus insecticides tend to be regarded as a homogeneous single entity. We aimed to determine whether organophosphate poisoning differs by subgroups in clinical features and severity. Methods: We retrospectively reviewed medical records of all patients with acute organophophorus poisoning from January 1998 to December 2006. We investigated clinical features, Glasgow coma scale (GCS), laboratory findings, QTc intervals, management, and outcomes. Results: A total of 109 patients were included. The dimethoxy group experienced significantly longer times than the diethoxy group for ventilation duration (0.6 day vs. 0.2 day, p=0.006), ICU duration (2.0 day vs. 0.8 day, p=0.037), and total admission duration (2.8 day vs. 0.9 day, p=0.008), except in cases of dichlorvos poisoning. Also, the GCS of the dimethoxy group (except with dichlorvos) was significantly lower than for the diethoxy group (dimethoxy, $11.2{pm}5.2$ vs. diethoxy, $13.8{pm}2.4$, p= 0.021). QTc intervals for the dimethoxy group (except with dichlorvos) tended to be somewhat greater than for the diethoxy group (dimethoxy, $452.9{pm}16.1;msec$ vs. diethoxy, $429.6{pm}40.9;msec$). There were 65 patients with dichlorvos ingestion, and 2 of these patients (3%) died. Conclusion: When compared to the diethoxy group, the dimethoxy group of organophosphates (with the exception of dichlorvos) were associated with poorer prognostic value for indicators such as GCS, QTc interval, requirement for intubation, ICU duration, and total admission duration. Within the dimethoxy group, patients with dichlorvos poisoning had relatively better prognoses than for the other dimethoxy group organophosphates studied.