No statistical difference was observed in serum venom levels (372; IQR 153.5C611.5 vs. the curve were: initial limb swelling, 0.88; demonstration time serum level, 0.80; initial necrosis, 0.75; individual demonstration time, 0.70. Serum venom level only cannot be used like a predictive element. The development of cells necrosis might be associated with the venom element, time element, and their connection. These influential factors can be used in future studies to PI3K-alpha inhibitor 1 evaluate antivenom effectiveness. and in Taiwan), Taiwan cobra envenomation causes more serious wound complications, such as local cells swelling and PI3K-alpha inhibitor 1 necrosis (Number 1), with few PI3K-alpha inhibitor 1 neurotoxic symptoms [9,10,11]. Cytotoxins of the three-finger toxin family are thought to cause wound necrosis after cobra bites [12]. It is also approved that higher cytotoxin doses may induce more considerable cells necrosis [13]. Open in a separate windowpane Number 1 An example of limb swelling and wound necrosis after Taiwan cobra bites. (Remaining): lower lower leg swelling progressively to the right knee joint. (Right): a necrosis wound was observed at the 3rd toe. Physicians use the bivalent freeze-dried neurotoxic antivenom PI3K-alpha inhibitor 1 (FNAV) produced by the Centers for Disease Control of Taiwan to treat cobra bites. The proposed roles of this FNAV antivenom treatment are to reduce limb swelling and prevents cells necrosis. However, even with large antivenom doses, as recommended from the Taiwan poison control center, the prevalence of wound necrosis and surgical procedures, such as debridement, remains high [11,12,13,14,15]. In Hungs earlier study, the authors observed that serum venom concentrations were suitable for differentiating between severe and slight envenomation [16]. However, the authors did not determine the relationship between serum venom concentration and the event of cells necrosis in their previous work. We hypothesize a correlation between the serum venom level and tissue necrosis development after cobra bites. Based on the aforementioned hypothesis, we investigated the factors influencing (including serum venom level) local tissue necrosis after cobra bites. 2. Results 2.1. Patient Characteristics There were 27 patients (6 men and 21 women) enrolled in this study (Table 1). We divided these 27 patients into wound necrosis and no wound necrosis groups according to whether wound necrosis designed or not. The median ages of the wound necrosis and no wound necrosis groups Rabbit Polyclonal to GHITM were not significantly different (45.5; IQR 33.5C61.5 vs. 48; IQR 34C59, = 0.99). Except for one patient who was bitten on the face, all patients were bitten around the limbs (17 upper limbs, 9 lower limbs). Systemic symptoms were observed in 16 of the 27 patients (59.2%). Of those 16, 7 patients demonstrated neurological muscle mass weakness (serum venom level: 228C1270 ng/mL), and 9 patients showed gastrointestinal symptoms. In contrast, 11 patients presented with local symptoms. There was no statistically significant difference between the wound necrosis and no wound necrosis groups in the systemic symptoms (= 0.14 and 0.37 for neurological and gastrointestinal symptoms, respectively). Table 1 Clinical characteristics and their comparisons between wound necrosis and no wound necrosis groups. = 8; (%)= 19; (%)= 0.0066, Wilcoxon rank-sum test). There were no ICU admissions or any other life-threatening conditions related to the snake bite in these patients. 2.2. Influential Factors of Local Tissue Necrosis 2.2.1. Patient Groups According to Presentation Time and Clinical SeverityWe divided the patients into three groups according to their presentation times and clinical severity. Group I, the early and mild presentation cases (cases 1C10, except case 7, with a PI3K-alpha inhibitor 1 presentation time of 7 h) received antivenom within 6 h (medium, 2.25 h; IQR, 2C4; range, 1 to 7 h; Physique 1). In summary, patients with low venom concentration/weight who received antivenom did not develop necrosis. Group II (cases 11C19) was the patient group with early presentation (6 h) with higher serum venom levels and moderate to severe presentation. They received 0C15 vials of antivenom administered.
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