■摄入黄磷杀鼠剂导致的急性肝衰竭通常是致命的。本研究旨在分析人口学特征和预后指标,重点关注高乳酸血症作为黄磷杀鼠剂中毒患者死亡率的潜在早期指标。
■这是一项回顾性研究,对96名含黄磷的杀鼠剂中毒的患者进行了回顾性研究(Ratol糊剂,其中含有3%的黄磷)。我们检查了人口统计细节,临床症状,和生化指标,以确定预后指标。
■幸存者和非幸存者的人口统计相似。死亡率(36.5%)与更高的摄入剂量和治疗延迟相关,死亡患者的平均存活天数(±SD)为5.26±2.2天。症状,包括胃肠和神经特征,通常在摄入后48小时出现。非幸存者的转氨酶活性增加(74.3%),凝血酶原时间延长(65.7%),住院期间高胆红素血症(65.7%),与幸存者相比,更常见(P<0.0001)。高乳酸血症(乳酸浓度>2mmol/L)存在于97.1%的非幸存者,在88.6%中观察到系列乳酸浓度增加。非幸存者入院乳酸浓度中位数(四分位数范围)为4.6mmol/L(3.36-7.53mmol/L),并且它们的峰值中位数(四分位数范围)乳酸浓度为6.1mmol/L(8.74-10.6mmol/L)。在非幸存者中,乳酸浓度的增加先于氨基转移酶活性的增加和凝血酶原时间的延长。Logistic回归和受试者工作特征曲线分析证实,24h乳酸浓度≥2.67mmol/L预测死亡的敏感性为94.3%,特异性为91.8%。
大多数摄入黄磷的患者最初无症状,通常在胃肠道症状发作后住院,通常是一天后。由于在大多数情况下,在摄入黄磷后的一周内发生死亡进展,尽早确定预后,可以迅速转诊至肝移植中心。根据我们的研究,24h乳酸浓度≥2.67mmol/L似乎是死亡的早期预后指标.在另一项研究中,乳酸浓度>5.8mmol/L是不良预后指标.
■入院时的高乳酸血症和连续乳酸浓度升高似乎是黄磷诱导的肝衰竭患者的早期不良预后体征。
UNASSIGNED: Acute hepatic failure due to yellow phosphorus rodenticide ingestion is often lethal. This study aimed to analyze demographic characteristics and prognostic indicators, focusing on hyperlactataemia as a potential early indicator of mortality in patients poisoned with yellow phosphorus rodenticide.
UNASSIGNED: This was a retrospective study of 96 patients poisoned with a yellow phosphorus-containing rodenticide (Ratol paste, which contains 3% yellow phosphorus). We examined demographic details, clinical symptoms, and biochemical markers to identify prognostic indicators.
UNASSIGNED: Demographics were similar among survivors and non-survivors. Mortality (36.5%) correlated with a higher ingested dose and treatment delays, with a mean (±SD) of 5.26 ± 2.2 survival days among those who died. Symptoms, including gastrointestinal and neurological features, typically appeared 48 h after ingestion. Non-survivors developed increased aminotransferase activities (74.3%), prolonged prothrombin time (65.7%), and hyperbilirubinaemia (65.7%) during hospitalization, significantly more commonly compared to survivors (P < 0.0001). Hyperlactataemia (lactate concentration >2 mmol/L) was present in 97.1% of non-survivors, with increased serial lactate concentrations observed in 88.6%. The median (interquartile range) admission lactate concentration among non-survivors was 4.6 mmol/L (3.36-7.53 mmol/L), and their peak median (interquartile range) lactate concentration was 6.1 mmol/L (8.74-10.6 mmol/L). In non-survivors, an increased lactate concentration preceded increased aminotransferase activities and prolonged prothrombin time. Logistic regression and receiver operating characteristic curve analysis confirmed that a 24 h lactate concentration ≥2.67 mmol/L predicted death with 94.3% sensitivity and 91.8% specificity.
UNASSIGNED: The majority of patients who ingest yellow phosphorus remain asymptomatic initially and typically present to hospital following the onset of gastrointestinal symptoms, usually a day later. As progression to death occurs within a week of yellow phosphorus ingestion in most cases, determining prognosis as early as possible enables swift referral to a liver transplant centre. Based on our study, a 24 h lactate concentration ≥2.67 mmol/L appears to be an early prognostic indicator of death. In another study, a lactate concentration >5.8 mmol/L was found to be a poor prognostic indicator.
UNASSIGNED: Hyperlactataemia on admission and increased serial lactate concentrations appear to be early poor prognostic signs in patients with yellow phosphorus-induced liver failure.