Acute organophosphate insecticide poisoning can manifest 3 different phases of toxic effects, namely, acute cholinergic crisis, intermediate syndrome (IMS), and delayed neuropathy. Among them, IMS has been considered as a major contributing factor of organophosphate-related morbidity and mortality because of its frequent occurrence and probable consequence of respiratory failure. Despite a high incidence, the pathophysiology that underlies IMS remains unclear. Previously proposed mechanisms of IMS include different susceptibility of various cholinergic receptors, muscle necrosis, prolonged acetylcholinesterase inhibition, inadequate oxime therapy, downregulation or desensitization of postsynaptic acetylcholine receptors, failure of postsynaptic acetylcholine release, and oxidative stress-related myopathy. The clinical manifestations of IMS typically occur within 24 to 96 hours, affecting conscious patients without cholinergic signs, and involve the muscles of respiration, proximal limb muscles, neck flexors, and muscles innervated by motor cranial nerves. With appropriate therapy that commonly includes artificial respiration, complete recovery develops 5-18 days later. Patients with atypical manifestations of IMS, especially a relapse or a continuum of acute cholinergic crisis, however, were frequently reported in clinical studies of IMS. The treatment of IMS is mainly supportive. Nevertheless, because IMS generally concurs with severe organophosphate toxicity and persistent inhibition of acetylcholinesterase, early aggressive decontamination, appropriate antidotal therapy, and prompt institution of ventilatory support should be helpful in ameliorating the magnitude and/or the incidence of IMS. Although IMS is well recognized as a disorder of neuromuscular junctions, its exact etiology, incidence, and risk factors are not clearly defined because existing studies are largely small-scale case series and do not employ a consistent and rigorous definition of IMS. Without a clear understanding of the pathophysiology of IMS, specific therapy is not available. The prognosis of IMS, however, is likely to be favorable if respiratory failure can be promptly recognized and treated accordingly.

Introduction. Neonicotinoids are a relatively new class of insecticides. They exhibit agonistic effects at postsynaptic nicotinic receptors in insects and are believed to have low toxicity in humans. Methods. We conducted a retrospective analysis of all neonicotinoid exposures reported to the Taiwan National Poison Center to better understand the toxicity profile of neonicotinoid insecticides. Results. A total of 70 patients were analyzed. Most exposures involved suicidal ingestions of imidacloprid alone. Clinical manifestations of neonicotinoid insecticide toxicity bear some resemblance to those of acute nicotine poisoning. Although most exposures were of mild-to-moderate severity, eight patients developed major effects and two died. Aspiration pneumonia and respiratory failure were the main cause of severe toxicity. Conclusion. Significant toxicity of neonicotinoids can occur following large amount of oral ingestion. Poisoned patients may present with cholinergic syndrome, and judicious use of atropine seems justified. Symptomatic treatment, especially ventilator support, remains most important in clinical management.

Background: Naja atra snakebite is uncommon in Taiwan and causes distinct effects on its victims. Although the Taiwan government produces its own specific antivenom, little information on the management of N. atra snakebite is available. Materials and methods: We retrospectively evaluated 183 patients admitted to two medical centers. Of these, 45 were identified as definite cases of N. atra snakebite, 86 as suspected cases, and 52 as clinical cases. Demographic data, symptomatology, and management were compared between these case groups. Results: Symptomatology and management were similar in the three groups. Among the 183 patients, 10 (5.5%) were asymptomatic and nine (4.9%) had transient and partial ptosis or body weakness. The principal effects were local tissue swelling and pain in 173 patients (94.5%), followed by clinically suspected wound infection in 148 (80.9%), skin necrosis in 120 (65.6%), necrotizing soft tissue infection in 77 (42.1%), fever in 59 (32.2%), and gastrointestinal effects in 53 (29%). The median total dose of specific antivenom needed to treat N. atra envenoming was 10 vials. In the envenomed patients, debridement was required in 74 patients (42.8%), fasciotomy/fasciectomy in 46 (26.6%), and finger or toe amputation in seven (4%). The first operation was performed at a median of 3.5 days after the bite. Discussion and conclusions: Based on these typical manifestations, clinical diagnosis of N. atra snakebites may be feasible and practical. In contrast to other snakes of Elapidae family, N. atra bite did not cause serious neurological effects. Early surgical consultation should be obtained because half of the patients underwent surgery due to infectious complications. Acute compartment syndrome was the surgical indication in rare cases; however, overestimation of the incidence may have occurred. This syndrome should be confirmed by serial intracompartmental pressure monitoring instead of only physical examination, and a sufficient dose of antivenom should be given prior to surgical decompression.

A total of 112 cases of Naja atra envenomation were examined at two referring hospitals: Taichung Veterans General Hospital in central Taiwan and Taipei Veterans General Hospital (VGH-TP) in northern Taiwan. Overall, 77% (86/112) of cases developed clinically suspected wound infections and 54% (61/112) required surgery secondary to tissue necrosis, finger or toe gangrene, and/or necrotizing fasciitis. Morganella morganii was the most abundant gram-negative bacterial strain isolated from bite wounds, followed by Proteus spp., Aeromonas hydrophila, Pseudomonas aeruginosa, and Providencia spp. in descending order; Enterococcus spp. were the most common gram-positive bacteria and Bacteroides spp. were the only anaerobic bacteria. A few episodes of bacteremia were caused by Bacteroides and Shewanella spp. There were no significant variations in the distribution of bacterial species between these two hospitals except for a higher incidence of M. morganii, Enterococcus spp., and polymicrobial infection observed at VGH-TP, which may have been related to variations in the fecal flora of prey and oral flora of individual snakes in different geographic areas in Taiwan. According to the susceptibility test involving various pathogens, first-line drug options for the management of N. atra snakebite wound infections may include monotherapy with ureidopenicillin or combination therapy with aminopenicillin and a third-generation cephalosporin or fluoroquinolone. A prospective evaluation of empiric antibiotic therapy for the management of N. atra snakebite should be considered.

Background. Glufosinate-containing herbicides are commonly used worldwide. Data on acute human glufosinate poisoning however remain scarce. Methods. We retrospectively reviewed the medical records of all glufosinate poisoned cases reported to the Taiwan National Poison Control Center and two medical centers in Taiwan from August 1993 through February 2010. Their demographic and clinical data were then analyzed to identify potential predictors of severe effects following acute glufosinate poisoning. Results. One hundred and thirty-one patients, including 115 oral and 16 non-oral exposures, were eligible for final analysis. Among patients with oral exposure, 25 were asymptomatic, while the others developed gastrointestinal, neurological, cardiovascular, and/or respiratory manifestations. Seven patients (6.1%) died following deliberate glufosinate ingestion. The median dose of glufosinate ingestion was 30.4 grams (interquartile range 18.5–45.6 grams) in the severe/fatal group compared to 6.8 grams (interquartile range 3.7–16.2 grams) in the non-severe group (p <0.001). Older age (≥61 years; adjusted OR 4.9, 95% CI 1.3–17.9) and larger amount of glufosinate ingestion (≥13.9 grams; adjusted OR 25.2, 95% CI 4.8–132.5) were positively associated with the development of severe toxicity, whereas ethanol consumption (adjusted OR 0.1, 95% CI <0.1–0.5) was inversely associated with the risk of severe toxicity. Conclusion. Although glufosinate is generally thought to be of low toxicity to humans, severe effects can occur and may be associated with older age, larger amount of ingestion and absence of concomitant ethanol consumption.

Macrocyclic lactones, including avermectins and milbemycins, are novel parasiticides and insecticides that are produced through fermentation by soil-dwelling microorganisms. Although various macrocyclic lactones may differ in their potency and safety, all of them are believed to share common pharmacologic/toxicologic mechanisms, i.e. leading to paralysis and death of parasites and other target organisms via the activation of a glutamate-gated chloride channel in the invertebrate nerve and muscle cells and/or through the effect on gamma-aminobutyric acid (GABA) receptors. Ivermectin is the first macrocyclic lactone that was released for use in both animals and humans, and has demonstrated both excellent efficacy and high tolerability in the treatment of parasite infestations. Other macrocyclic lactones, such as abamectin, emamectin, and moxidectin were subsequently commercialized and have been used as insecticides and acaricides for crop protection or parasiticides for animal health. Although ivermectin therapy is generally well tolerated, adverse effects that are usually transient and mild-to-moderate can occur. Severe adverse effects are rare and can generally be effectively controlled by symptomatic measures. Non-therapeutic exposures to ivermectin and other macrocyclic lactones may also result in toxic effects; significant toxicity however probably develops only after large amount of oral ingestion. Although the exact mechanisms remain unclear, macrocyclic lactones in large doses may pass through the blood-brain barrier (BBB) to produce GABA-mimetic toxic effects. Severely poisoned patients usually present with coma, hypotension, respiratory failure, and even death. Despite the lack of specific therapy, the prognosis is likely to be favorable unless the poisoned patients are complicated with severe hypotension or respiratory failure.