Respiratory failure in acute organophosphorus pesticide self-poisoning

BACKGROUND: Acute organophosphorus (OP) pesticide poisoning is a major clinical problem in the developing world. Textbooks ascribe most deaths to respiratory failure occurring in one of two distinct clinical syndromes: acute cholinergic respiratory failure or the intermediate syndrome. Delayed failure appears to be due to respiratory muscle weakness, but its pathophysiology is unclear. AIM: To describe the clinical patterns of OP-induced respiratory failure, and to determine whether the two syndromes are clinically distinct. DESIGN: Prospective study of 376 patients with confirmed OP poisoning. METHODS: Patients were observed throughout their admission to three Sri Lankan hospitals. Exposure was confirmed by butyrylcholinesterase and blood OP assays. RESULTS: Ninety of 376 patients (24%) required intubation: 52 (58%) within 2 h of admission while unconscious with cholinergic features. Twenty-nine (32%) were well on admission but then required intubation after 24 h while conscious and without cholinergic features. These two syndromes were not clinically distinct and had much overlap. In particular, some patients who required intubation on arrival subsequently recovered consciousness but could not be extubated, requiring ventilation for up to 6 days. DISCUSSION: Respiratory failure did not occur as two discrete clinical syndromes within distinct time frames. Instead, the pattern of failure was variable and overlapped in some patients. There seemed to be two underlying mechanisms (an early acute mixed central and peripheral respiratory failure, and a late peripheral respiratory failure) rather than two distinct clinical syndromes.     

Acid-base interpretation can be the predictor of outcome among patients with acute organophosphate poisoning before hospitalization

Objectives

Acute organophosphate (OP) poisoning causing alteration in acid-base equilibrium was reported before. Hence, different acid-base statuses may present in patients with acute poisoning due to OP exposure. This study aims to determine the impact of acid-base interpretation in patients with acute OP poisoning before hospitalization in medical care units and to describe the pattern of mortality with different acid-base statuses.

Design and Patients

Over a 9-year retrospective study, from July 1996 to August 2005, a total of 82 consecutive patients with acute OP poisoning were admitted to the China Medical University Hospital (Taichung, Taiwan) within 24 hours after exposure to OP and were enrolled into this study.

Results

Patients with acute OP poisoning were divided into 4 groups: without acidosis, metabolic acidosis, respiratory acidosis, and mixed acidosis. Overall survival (Kaplan-Meier curves) among groups was statistically significant (P < .0001). The mortality rate of acute OP poisoned patients with metabolic acidosis was 25%, and 75% of those patients died of cardiovascular failure. The mortality rate of acute OP poisoning with respiratory acidosis was 50%, and 50% of those patients died of respiratory failure.

Conclusions

Acid-base interpretation can be effective in quick diagnosis and prediction of the outcome of patients with acute OP poisoning (without acidosis < metabolic acidosis < respiratory acidosis < mixed acidosis) before hospitalization. Major causes of death are different between the respiratory acidosis and metabolic acidosis groups of patients with acute OP poisoning.     

Survival Pattern in Patients with Acute Organophosphate Poisoning Receiving Intensive Care

Background. Approximately 35% of patients acutely poisoned with organophosphates (OP) in developing countries like Sri Lanka require intensive care and mechanical ventilation. However, death rates remain high. Objective. To study the outcomes and predictors of mortality in patients with acute OP poisoning requiring intensive therapy at a regional center in Sri Lanka over a period of 40 months. Methods. Retrospective analysis of all intensive care records of patients with acute OP poisoning admitted to the Intensive Care Unit (ICU) between March 1998 and July 2001. Results. During the study period, 126 subjects were admitted to the ICU with acute OP poisoning. Records of 10 patients were lost and those of 37 were incomplete and hence were excluded. All the remaining 71 patients (59 male) had required endotracheal intubation and mechanical ventilation for a period of four (median) days (range 1–27) in addition to gastric lavage and standard therapy with atropine and oximes and adequate hydration. Of these 71 patients, 36 (28 male) had died. Life table analysis demonstrated a steep decline in the cumulative survival to 67% during the first three days. Systolic blood pressure of < 100 mmHg and FiO₂ of > 40% to maintain a SpO₂ of > 92% within the first 24 h were recognized as poor prognostic indicators among mechanically ventilated patients. Conclusion. Mortality following OP poisoning remains high despite adequate respiratory support, intensive care, and specific therapy with atropine and oximes. One‐third of the subjects needing mechanical ventilation and reaching intensive care units die within the first 72 h of poisoning. Systolic blood pressure of less than 100 mmHg and the necessity of a FiO₂ > 40% to maintain adequate oxygenation are predictors of poor outcome in patients mechanically ventilated in the ICU.     

Prognostic value of serial serum cholinesterase activities in organophosphate poisoned patients

Objectives

Organophosphate (OP) poisoning is a worldwide concern. Several factors have been identified to predict outcomes of OP poisoned patients. This study focuses on the relationship between the trend in Serum cholinesterase (SChE) activity and its clinical outcome in acute OP poisoned patients.

Methods

We retrospectively reviewed the medical records of all adult acute OP poisoned patients that visited the Emergency Department from 2000 to 2006. These patients were divided into two groups: the deceased patients as the sample group and all others as the control group. We collected data on the following: demographical factors, poisoning history, clinical manifestation, Glasgow Coma Scale (GCS), APACHE II score, all SChE data within 48 hours, hourly 2-PAM dosage, intubation, and mortality. Chi-Square test then examined the relationship between the trend of SChE activity and mortality.

Results

86 patients were enrolled. Follow-up measurements of SChE activity within 48 hours of poisoning were available in 50 cases. Among these, eight patients died. We found no significant difference between the sample and control groups on initial SChE activity, time interval to initial SChE data, and hourly 2-PAM dosage. The sampled group possessed a worse GCS score, lower systolic blood pressure, and a higher APACH II score. Increase patient mortality rates associated with the absence of elevating SChE activity within 48 hours of poisoning. (P = .006, odds ratio:11).

Conclusions

We propose that the absence of elevating SChE activity level within 48 hours of poisoning appears to associate with higher mortality in acute OP poisoned patients.     

Detectable serum ethylene glycol levels after subcutaneous injection of antifreeze

Context. Paraquat is a widely used herbicide that can cause severe to fatal poisoning in humans. The irreversible and rapid progression of pulmonary fibrosis associated with respiratory failure is the main cause of death in the later stages of poisoning. There are infrequent reports of successful lung transplants for cases of severe paraquat poisoning. We expect that this successful case will provide a reference for other patients in similar circumstances. Case details. A 24-year-old female was sent to the hospital approximately 2 hours after ingesting 50 ml of paraquat. She experienced rapidly aggravated pulmonary fibrosis and severe respiratory failure. On the 34th day after ingestion, she underwent intubation and invasive mechanical ventilation. The patient was evaluated for lung transplantation, and veno-venous extracorporeal membrane oxygenation (ECMO) was established as a bridge to lung transplantation on the 44th day. On the 56th day, she successfully underwent a bilateral sequential lung transplantation. Through respiratory and physical rehabilitation and nutrition support, the patient was weaned from mechanical ventilation and extubated on the 66th day. On the 80th day, she was discharged. During the 1-year follow-up, the patient was found to be in good condition, and her pulmonary function improved gradually. Conclusion: We suggest that lung transplantation may be an effective treatment in the end stages of paraquat-induced pulmonary fibrosis and consequential respiratory failure. For patients experiencing a rapid progression to a critical condition in whom lung transplantation cannot be performed immediately (e.g., while awaiting a viable donor or toxicant clearance), ECMO should be a viable bridge to lung transplantation.     

Features of myocardial injury in severe organophosphate poisoning

Background. In organophosphate (OP) poisoning cardiac complications may occur. However, the current body of knowledge largely consists of limited studies, and case reports are mainly on electrocardiogram (ECG) abnormalities. As definite myocardial injury is difficult to assess through ECG, we investigated the prevalence of myocardial injury through cardiac biochemical markers such as troponin I (TnI) in severe OP poisoning. Methods. We conducted a retrospective review of 99 consecutive OP insecticide poisoning cases that were diagnosed and treated at the emergency department of the Wonju Severance Christian Hospital between March 2008 and December 2013. Results. Based on Namba classification for OP poisoning, there were no patients with mild toxicity, 9 patients (9.1%) with moderate toxicity and 90 patients (90.9%) with severe toxicity. On ECG, normal sinus rhythm was most common, and ST depression and elevation were seen in 11 patients (11.1%). Elevation of TnI within 48 h was seen in 34 patients (34.3%). The median peak level and peak time of TnI were 0.305 (IQR, 0.078–2.335) ng/mL and 15 (IQR 6.9–34.4) hours, respectively. There were differences between patients with normal TnI and elevated TnI in terms of age (yrs), number of patients who were exposed to OP via the oral route, and initial Glasgow Coma Scale (GCS; 58 ± 17 vs. 66 ± 16, p = 0.015, 56 [87.5%] vs. 33 [97.1%], p = 0.048 and 12.0 [IQR, 8.0–15.0] vs. 9.0 [IQR, 5.8–12.0], p = 0.019). Conclusions. OP can cause direct myocardial injury during the acute early phase in severe OP poisoning. Monitoring of TnI may be needed in severe OP poisoning.     

Acute Ethylene Chlorohydrin Poisoning: Experience of a Poison Control Center

Background: Ethylene chlorohydrin (CAS 107-07-3), a chemical once used in hastening grape vine sprouting in Taiwan, has caused severe toxicity upon acute exposure. Although such use of ethylene chlorohydrin is now prohibited in Taiwan, poisoning still occurs following its illegal use. Since data concerning human ethylene chlorohydrin poisoning remain rare, we report our experience in treating acute ethylene chlorohydrin–poisoned patients. Methods: A retrospective analysis was conducted to evaluate patients with ethylene chlorohydrin poisoning reported to Taiwan Poison Control Center during 1985–1998. Results: Seventeen patients with ethylene chlorohydrin poisoning were identified. There were 11 male and 6 female patients, ranging in age from 2 to 70 years (median 53 years). The intent of exposure was suicide in 5, accident in 9, and occupational exposure in 3 patients. Oral ingestion was the most common route of exposure (14 patients). Seven out of the 17 patients died within 24 hours due to metabolic acidosis and respiratory failure. Ethanol therapy, used in 2 patients, had no apparent benefit. Moderate or mild poisoning was characterized by gastrointestinal effects only and an uneventful recovery. Conclusions: Ethylene chlorohydrin can result in severe metabolic acidosis, respiratory failure, coma, and death after acute exposure.     

Incidence et caractéristiques des intoxications graves au méthomyl (carbamate anticholinestérasique) à l'île de la Réunion

Objective: To define the incidence and characteristics of acute poisoning by methomyl (Lannate 20 L® ingestion.Design: Retrospective epidemiologic study based on medical records from the Hospital Sud Reunion on Reunion Island between June 1991 and March 1995.Recruitment of cases: Any patient poisoned by ingestion of Lannate 20 L®.Results: Fifty-six poisonings were listed, among which 42 males aged 40 ± 13.2 years old and 14 females aged 31 ± 12.5 years old. The ingested dose was estimated at 50 ml Lannate 20 L for six patients (142.8 mg/kg), and was unknown for the others. Twelve patients deceased before hospital admission. Among the 44 other victims, 25% presented a muscarinic syndrome, 27% a ganglionic nicotinic syndrome, 70% a CNS syndrome (coma) and 77.3% a respiratory distress syndrome. Thirty-six patients (82%) had a blood level of pseudocholinesterases below 2,000 UI/L. Thirty-five patients required immediate intubation and ventilation. The mean atropine dose required by 42 patients was 38.5 + 42.6 mg over the first 24 ± 33 hours. Nine patients died in the intensive care unit.Conclusions: Poisoning by methomyl has to be treated in intensive care units. Atropine remains the first-line treatment and oximes are not yet systematically used in this indication.     

Assessment of the severity of organophosphate (fenitrothion) poisoning based on its serum concentration and clinical parameters

Background. Fenitrothion (MEP) is the most frequent cause of organophosphate pesticides (OP) poisoning in Japan, but clinical parameters to predict its severity remain uncertain. Method. We evaluated 26 cases (12 males and 14 females) of MEP poisoning brought to our critical care center. Regarding acute lung injury (ALI) as a hallmark complication leading to poor recovery, we divided patients into two groups: cases without ALI (Grp1, n = 14), and cases who developed ALI (Grp2, n = 12) at various points after the poisoning. Serial changes in clinical parameters and laboratory test results were compared between them. Results. The median MEP concentrations on arrival (min～max) for Grp1 and Grp2 were 2.3 (0.5–5.1) and 4.6 (1.1–14.0) μg/ml, respectively. Serum pseudo-cholinesterase (PChE) levels on arrival were 21(< 10–59) U/L in Grp1 and < 10 in Grp2. Based on individual patient kinetics, we estimated MEP concentration at 2 and 24 hours after ingestion, and determined cutoff values for differentiating the two groups for each time point as 4.0 μg/ml and 0.5 μg/ml, respectively. By logistic regression analysis, two groups were distinguished with accuracy of 92.3% based on their time of arrival after ingestion and initial MEP concentration. Clinical parameters associated with ALI were days with miosis, days with PChE below 100 U/L, and days requiring administration of atropine. Conclusion. The severity of MEP poisoning is closely associated with both time to presentation after ingestion and initial MEP concentration. Serial monitoring of MEP concentrations in the first 24 hours is also useful in predicting the clinical course.     

急性有机磷中毒继发中间综合征的观察与护理

目的：研究急性有机磷中毒继发中间综合征（IMS）的护理。方法：采取有效的急救与护理措施,治疗护理有机磷中毒8例。结果：8例中6例安全渡过缺氧危象期,无合并肺部、口腔、尿路感染,分别于IMS后10－28d痊愈出院。1例因合并多脏器功能衰竭,1例因中毒程度深,发生IMS后抢救无效死亡。结论：对急性有机磷中毒恢复期患,需严密观察有无IMS早期征象,肌无力症状和胆碱酯酶活性（chE),并与反跳、周围性呼衰及中枢性呼衰相鉴别;及时气管插管、气管切开,应用呼吸机人工辅助呼吸,维持有效的呼吸功能及氧疗是抢救成功的关键,同时做好呼吸道与呼吸机的护理及管理,预防感染等并发症的发生。     

Acute Endosulfan Poisoning with Cerebral Edema and Cardiac Failure

Background. Organochlorine insecticides are highly toxic compounds that are responsible for a number of severe intoxications worldwide with several deaths. Despite their widespread use in agriculture during the 1940s to 1960s and the well‐known signs and symptoms of intoxication, the clinical picture in case of poisoning varies. We report two cases of acute intentional endosulfan intoxication with cerebral edema and cardiac failure. Case Reports. Both cases developed life‐threatening signs like epileptic state, respiratory insufficiency and hemodynamic instability soon after ingestion. The survivor developed severe myocardial insufficiency and pulmonary edema documented by echocardiography and x‐ray of the chest. The deceased patient developed severe cerebral edema and multiorgan failure ten days after ingestion of Thiodan® 35. The peak serum concentration of endosulfan in the survivor was 0.12 mg/L approximately 23 hours after ingestion, whereas the peak blood concentration in the fatal case was 0.86 mg/L approximately 25 hours post‐ingestion. Post‐mortem endosulfan levels in different organs were determined. Conclusion. Endosulfan is a highly toxic organochlorine insecticide that produces well‐known neurological symptoms of tonic‐clonic convulsions, headache, dizziness and ataxia but also can cause gastrointestinal symptoms and metabolic disturbances. Life‐threatening cerebral edema and hemodynamic instability may occur. Treatment is symptomatic and supportive.     

Case report: severe mercuric sulphate poisoning treated with 2,3-dimercaptopropane-1-sulphonate and haemodiafiltration

Introduction

Inorganic mercury poisoning is uncommon, but when it occurs it can result in severe, life-threatening features and acute renal failure. Previous reports on the use of extracorporeal procedures such as haemodialysis and haemoperfusion have shown no significant removal of mercury. We report here the successful use of the chelating agent 2,3-dimercaptopropane-1-sulphonate (DMPS), together with continuous veno-venous haemodiafiltration (CVVHDF), in a patient with severe inorganic mercury poisoning.

Case report

A 40-year-old man presented with haematemesis after ingestion of 1 g mercuric sulphate and rapidly deteriorated in the emergency department, requiring intubation and ventilation. His initial blood mercury was 15 580 μg/l. At 4.5 hours after ingestion he was started on DMPS. He rapidly developed acute renal failure and so he was started on CVVHDF for renal support and in an attempt to improve mercury clearance; CVVHDF was continued for 14 days.

Methods

Regular ultradialysate and pre- and post-filtrate blood samples were taken and in addition all ultradialysate generated was collected to determine its mercury content.

Results

The total amount of mercury in the ultrafiltrate was 127 mg (12.7% of the ingested dose). The sieving coefficient ranged from 0.13 at 30-hours to 0.02 at 210-hours after ingestion. He developed no neurological features and was discharged from hospital on day 50. Five months after discharge from hospital he remained asymptomatic, with normal creatinine clearance.

Discussion

We describe a patient with severe inorganic mercury poisoning in whom full recovery occurred with the early use of the chelating agent DMPS and CVVHDF. There was removal of a significant amount of mercury by CVVHDF.

Conclusion

We feel that CVVHDF should be considered in patients with inorganic mercury poisoning, particularly those who develop acute renal failure, together with meticulous supportive care and adequate doses of chelation therapy with DMPS.     

Utility of Hypertonic Saline and Diazepam in COVID-19–Related Hydroxychloroquine Toxicity

BackgroundHydroxychloroquine (HCQ) poisoning is a life-threatening but treatable toxic ingestion. The scale of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection (COVID-19) and the controversial suggestion that HCQ is a treatment option have led to a significant increase in HCQ use. HCQ poisoning should be at the top-of-mind for emergency providers in cases of toxic ingestion. Treatment for HCQ poisoning includes sodium bicarbonate, epinephrine, and aggressive electrolyte repletion. We highlight the use of hypertonic saline and diazepam.Case ReportWe describe the case of a 37-year-old man who presented to the emergency department after the ingestion of approximately 16 g of HCQ tablets (initial serum concentration 4270 ng/mL). He was treated with an epinephrine infusion, hypertonic sodium chloride, high-dose diazepam, sodium bicarbonate, and aggressive potassium repletion. Persistent altered mental status necessitated intubation, and he was managed in the medical intensive care unit until his QRS widening and QTc prolongation resolved. After his mental status improved and it was confirmed that his ingestion was not with the intent to self-harm, he was discharged home with outpatient follow-up.Why Should an Emergency Physician Be Aware of This?For patients presenting with HCQ overdose and an unknown initial serum potassium level, high-dose diazepam and hypertonic sodium chloride should be started immediately for the patient with widened QRS. The choice of hypertonic sodium chloride instead of sodium bicarbonate is to avoid exacerbating underlying hypokalemia which may in turn potentiate unstable dysrhythmia. In addition, early intubation should be a priority in vomiting patients because both HCQ toxicity and high-dose diazepam cause profound sedation.     

End expiratory oxygen concentrations to predict central venous oxygen saturation: an observational pilot study

Background

Organophosphorus (OP) pesticide poisoning is the most common form of pesticide poisoning in many Asian countries. Guidelines in western countries for management of poisoning indicate that gastric lavage should be performed only if two criteria are met: within one hour of poison ingestion and substantial ingested amount. But the evidence on which these guidelines are based is from medicine overdoses in developed countries and may be irrelevant to OP poisoning in Asia. Chinese clinical experience suggests that OP remains in the stomach for several hours or even days after ingestion. Thus, there may be reasons for doing single or multiple gastric lavages for OP poisoning. There have been no randomised controlled trials (RCTs) to assess this practice of multiple lavages. Since it is currently standard therapy in China, we cannot perform a RCT of no lavage vs. a single lavage vs. multiple lavages. We will compare a single gastric lavage with three gastric lavages as the first stage to assess the role of gastric lavage in OP poisoning.

Methods/Design

We have designed an RCT assessing the effectiveness of multiple gastric lavages in adult OP self-poisoning patients admitted to three Chinese hospitals within 12 hrs of ingestion. Patients will be randomised to standard treatment plus either a single gastric lavage on admission or three gastric lavages at four hour intervals. The primary outcome is in-hospital mortality. Analysis will be on an intention-to-treat basis. On the basis of the historical incidence of OP at the study sites, we expect to enroll 908 patients over three years. This projected sample size provides sufficient power to evaluate the death rate; and a variety of other exposure and outcome variables, including particular OPs and ingestion time. Changes of OP level will be analyzed in order to provide some toxic kinetic data.

Discussion

the GLAOP study is a novel, prospective cohort study that will explore to the toxic kinetics of OP and effects of gastric lavage on it. Given the poor information about the impact of gastric lavage on clinical outcomes for OP patients, this study can provide important information to inform clinical practice.     

Delayed Neurologic Sequelae Resulting from Epidemic Diethylene Glycol Poisoning

Background. Diethylene glycol (DEG) is a well-known metabolic and renal toxin usually ingested accidentally as an ethanol substitute or as a contaminant in various medicinals. To date, most poisonings have occurred in third-world countries where early death from renal failure is very common. We report a series of seven patients presenting with epidemic DEG poisoning from a correctional facility with varying degrees of metabolic acidemia and acute renal impairment responding to emergent hemodialysis (HD). Significantly, three patients developed delayed neurologic toxicity which has not been well characterized in the past. Case Series. Seven male patients (age range 19–55) presented over a 36 h period following ingestion of varying quantities of DEG. Initially three patients, ingesting the largest quantities of DEG, presented more than 24 h postingestion with severe metabolic acidemia (pH range 6.8–7.1) and anuric acute renal failure requiring HD. All three remained dialysis-dependent and developed significant cranial neuropathies with bulbar palsy in the second week postingestion. One patient died with cerebral oedema and a progressive encephalopathy. Two further patients presented within 24 h of ingestion with normal renal function and a moderate metabolic acidemia (pH range 7.2–7.28) requiring HD. They remained well. Finally, two further patients presented with a history of trivial DEG ingestion and did not require any therapy. Neurologic signs in the two surviving initial presenters improved over 4–6 months although they remained dialysis-dependent. Conclusion. Unrecognized DEG poisoning may present with metabolic acidemia and anuric acute renal failure. Established renal impairment may predict subsequent delayed neurologic toxicity.     

Effectiveness of therapeutic plasma exchange in patients with intermediate syndrome due to organophosphate intoxication

Objective

We aimed to determine effectiveness of therapeutic plasma exchange (TPE) in patients with intermediate syndrome (IMS) due to organophosphate (OP) intoxication.

Methods

Patients diagnosed with IMS due to OP intoxication were included in this prospective study. Therapeutic plasma exchange procedure was performed with fresh frozen plasma as a replacement fluid via Fresenius-AS-TEC 204 device by Therapeutic Apheresis Unit to patients who developed IMS during follow-up. Samples were taken from patient's blood and waste plasma collected in the device before and after TPE procedure to be studied in laboratory for detection of organic phosphate and pseudocholinesterase (PChE) levels. In this study, SPSS 18.0 software package was used for statistical analysis of the data obtained. Level of statistical significance was taken as P < .05 for all tests.

Results

Of all 17 patients, 4 (23.5%) were female, and 13 (76.5%) were male. A statistically significant decrease was detected in organic phosphate levels in the plasma of patients after TPE procedure (P = .012). A statistically significant increase was detected in PChE levels in the plasma of patients after TPE procedure (P = .014). Of 17 patients included in the study, 13 patients showed clinical improvement and were discharged after the TPE process.

Conclusion

In our study, it was observed that a significant decrease in the level of blood plasma OP and a significant increase in the level of PChE were achieved with TPE process in the early period of IMS due to OP poisoning. This study indicates that TPE is one of the effective treatment options for IMS due to OP intoxication.     

Glasgow Coma Scale Score and QTc Interval in the Prognosis of Organophosphate Poisoning

OBJECTIVES: The aim of this study was to assess the applicability of the Glasgow Coma Scale (GCS) score and the Q-T interval corrected for heart rate (QTc interval) in predicting outcome and complications in patients with organophosphate (OP) poisoning. METHODS: This prospective, observational study included 65 patients older than 18 years. In the out-of-hospital setting, the end-tidal carbon dioxide (ETCO2), oxygen saturation (SaO2), QTc interval, and GCS score were monitored in each patient. A statistical comparison was then made between the group with respiratory failure and the group without this complication. RESULTS: The group with complications had significantly different values of measured parameters--a longer QTc interval and a lower GCS score, a higher number of intubations, and worse outcomes (p < 0.05). The two measures, GCS score and QTc interval, have been shown to be equally good in predicting respiratory failure and hospital mortality in patients with OP poisoning. CONCLUSIONS: In the initial out-of-hospital care of patients with OP poisoning, it is essential to monitor QTc interval and GCS score. These measures help with prognosis, and may suggest when to initiate precautions to prevent complications (i.e., respiratory failure). The simplicity and promptness of these methods allow providers to perform early and effective triage.     

Toxicity Following Unintentional DDT Ingestion

Introduction: Dichlorodiphenyltrichloroethane (DDT) ingestion is an uncommon cause of poisoning worldwide. To date, no cases of renal impairment after oral intake of DDT in humans have been reported. We describe the clinical course and management of two patients presenting after DDT ingestion, one of whom developed acute oliguric renal failure. Case Report: A father and son mistook DDT powder for flour while preparing fish for a meal, and after eating they developed symptoms compatible with acute organochlorine insecticide poisoning. Both were intubated endotracheally due to recurrent convulsions and loss of consciousness followed by admission to the intensive care unit. Both cases developed severe metabolic acidosis. Acute oliguric renal failure (ARF) was diagnosed in the son in the second day, with a blood urea nitrogen level of 47 mg/dl and creatinine 6.4 mg/dl. Urinalysis disclosed abundant RBCs on the third day. Vigorous fluid resuscitation and strict monitoring helped reverse its clinical course by the tenth day. Both patients recovered within two weeks and were discharged without sequelae. Conclusion: Clinicians should not overlook the possibility of DDT poisoning in the differential diagnosis of acute renal failure and seizures. More strict measures should be taken to prohibit misidentification of DDT and similar products, particularly in the developing world.     

Diazepam Inhibits Organophosphate-induced Central Respiratory Depression

OBJECTIVES: Current evidence suggests that mortality from acute organophosphate (OP) poisoning is partially mediated through central nervous system (CNS) respiratory center depression (CRD). However, the exact mechanism of OP-induced CRD is unknown. In these studies, the authors investigated the hypothesis that OP-induced CRD is the result of overstimulation of CNS respiratory centers. METHODS: Wistar rats received prophylaxis with either normal saline (controls), atropine, the peripherally acting anticholinergics glycopyrrolate (GLYC), ipratropium bromide (IB), or the CNS respiratory center attenuator diazepam. To determine if a dual CNS/peripheral cholinergic mechanism is responsible for animal death, two additional groups received combination treatment with diazepam plus either IB or GLYC. All treatments were completed 5 minutes before OP with subcutaneous dichlorvos. Differences in 10-minute and 24-hour mortality were assessed by the Fisher exact test. RESULTS: Dichlorvos poisoning resulted in profound fasciculations without obvious seizure in all cohorts. In controls and animals treated with peripherally acting anticholinergics, fasciculations were followed by sedation and respiratory arrest (0% 10-minute survival in all cohorts). In contrast, pretreatment with either atropine or diazepam significantly improved 10-minute survival (100% and 44%, respectively). Although GLYC or IB afforded no protection when given alone, when delivered in conjunction with diazepam, the combination significantly improved survival (both groups 88% at 24 hours), suggesting a dual CNS/pulmonary muscarinic mechanism of lethality. CONCLUSIONS: The central respiratory depressant diazepam paradoxically attenuates organophosphate-induced respiratory depression, and when combined with peripherally acting anticholinergic agents, reduces mortality in a rat model of severe acute OP poisoning.     

预见性气管插管治疗急性重度药物中毒临床观察

目的:探讨重度药物中毒患者的气管插管时机对治疗效果的影响。方法:对57例出现呼吸困难的重度药物中毒患者,进行密切观察,在常规治疗的基础上,随机分为预见性气管插管组与延时气管插管组;以并发症发生情况及抢救成功率进行统计学处理,比较两组患者的抢救效果。结果:各种并发症发生情况两组比较P>0.05差异无统计学意义,可能与中毒的量及中毒时间有关;不同时机气管插管抢救成功率两组比较P<0.05,有一定的可比性。结论:预见性气管插管有助于重度药物中毒患者的抢救,气管插管最佳时机为呼吸衰竭早期。