不同类型急性乙醇中毒所致心脏损害分析

目的：探讨不同类型急性乙醇中毒所致心脏损害特点。方法：193例中毒者分为白酒、红酒及啤酒组,观察其心电图（ECG）及全血肌钙蛋白T定量（TNT）变化。结果：白酒组较红酒组、啤酒组ECG异常率及TNT增高率均有统计学差异（P〈0.05）。结论：饮用白酒所致急性中毒者可能更易发生心脏损害,临床工作中需加以注意并及时治疗。     

醒脑静654-2联合纳洛酮治疗重度急性酒精中毒

目的 观察醒脑静、654-2联用纳洛酮治疗重度急性酒精中毒的效果.方法 122例重度急性酒精中毒患者随机分成三组;醒脑静、654-2联合纳洛酮为Ⅰ组36例,654-2联合纳洛酮为Ⅱ组48例,单纯纳洛酮为Ⅲ组38例,观察三组治疗后患者的清醒时间.结果 三组清醒时间比较,Ⅰ组与Ⅱ组比较差异有统计学意义(P＞0.05),Ⅰ组、Ⅱ组与Ⅲ组比较差异有统计学意义(P＜0.001).结论 醒脑静、654-2联合纳洛酮治疗重度酒精中毒催醒效果明显优于单用纳洛酮,且比654-2联用纳洛酮治疗重度急性酒精中毒清醒时间短,具有比较理想的临床效果.     

纳洛酮联合醒脑静注射液在抢救急性重度酒精中毒的应用

目的探析纳洛酮联合醒脑静注射液在抢救急性重度酒精中毒患者中的效果。方法以我院急诊科2013年4月-2014年8月所收集85例急性重度酒精中毒患者为例,常规急诊处理基础上对照组应用纳洛酮,观察组加用醒脑静注射液,比较两组痊愈时间、显效时间、有效时间、出院时间及不良反应发生率。结果观察组有效时间、显效时间、痊愈时间、出院时间均短于对照组,差异比较有统计学意义（P〈0.05）。两组不良反应发生率为比较差异有统计学意义（P〈0.05）。结论醒脑静注射液联合纳洛酮抢救急性重度酒精中毒患者可发挥协同解毒作用而缩短患者醒转时间,不良反应更少,应用价值高。     

重度酒精中毒洗胃与非洗胃的疗效观察

目的探讨急性重度酒精中毒病人洗胃与非洗胃的疗效差异及护理措施。方法将药物治疗相同的洗胃组35例与非洗胃组72例急性重度酒精中毒病人的临床资料进行比较。结果两组病人的意识清醒时间与临床治愈时间无统计学差异。结论急性重度酒精中毒病人洗胃不缩短苏醒时间和临床治愈时间。     

急性重度有机磷农药中毒患者死亡危险因素分析

目的：探讨急性重度有机磷农药中毒死亡的危险因素。方法回顾性分析急性重度有机磷农药中毒44例患者的临床资料,对各项危险因素进行统计分析,比较患者的病死率。结果44例急性重度有机磷农药中毒患者住院期间病死率22.7%(10/44),其中急性生理学及慢性健康状况评分(APACHE)≥20分和<20分、年龄≥60岁和<60岁、合并低血压和未合并低血压、合并低氧血症和未合并低氧血症、合并代谢性酸中毒和未合并代谢性酸中毒的患者病死率比较,差异均有统计学意义(P <0.05或<0.01)。结论 APACHEⅡ分值、高龄、低血压、低氧血症、代谢性酸中毒可能是急性重度有机磷农药中毒患者死亡的危险因素,在临床中可以用于评估患者病情严重程度与死亡风险。     

早期血气分析对急性有机磷农药中毒患者预后的预测

目的 探讨急性有机磷农药中毒(AOPP)患者的酸碱平衡与死亡率的关系.方法 回顾性研究我院2000-01～2006-01在急诊科就诊并收入住院的78例连续的、中毒时间在24 h内的AOPP患者,依据第一次动脉血气结果 判断是否存在酸中毒及酸中毒类型,并对各类型的死亡率进行比较.结果 AOPP患者分为无酸中毒组、代谢性酸中毒组、呼吸性酸中毒组和混合型酸中毒组,组间死亡率比较差异有统计学意义(P＜0.01).有代谢性酸中毒的AOPP患者死亡率为22.5%,其中71.4%死于心力衰竭;有呼吸性酸中毒的AOPP患者死亡率为42.9%,其中66.7%死于呼吸衰竭.结论 酸碱度能有效预测AOPP患者的死亡率, 代谢性酸中毒组的死亡原因与呼吸性酸中毒组不同.     

糖尿病酮症酸中毒患者使用胰岛素泵安全性及有效性观察

目的观察胰岛素泵治疗糖尿病酮症酸中毒的临床疗效及安全性。方法选取我院2009年7月～2012年5月收治的60例糖尿病酮症酸中毒患者作为研究对象,按照随机数字表法随机分为观察组和对照组各30例,观察组采用胰岛素泵治疗,对照组采用小剂量胰岛素静脉滴注治疗,比较两组患者的血糖恢复时间、胰岛素用量、尿酮体转阴时间、血pH值恢复正常时间及低血糖发生率。结果 (1)两组患者胰岛素用量及血糖恢复正常时间比较并无明显差异(P>0.05),但尿酮体转阴时间及血pH值恢复时间比较有明显差异(P<0.05),具有统计学意义。(2)观察组低血糖1例(3.33%);对照组低血糖4例(13.3%)。两组患者低血糖发生率比较有明显差异(P<0.05),具有统计学意义。结论胰岛素泵治疗糖尿病酮症酸中毒效果理想,可以缩短尿酮体转阴及血pH值恢复时间,且安全性较高,值得推广应用。     

酒精中毒患者的阴离子间隙和渗透压阶差分析

随着经济的发展,居民社交增多,急性酒精中毒也呈增多趋势。国外文献报道,急性酒精中毒时酮症酸中毒发生率较高,酒精性酮症酸中毒是急诊科常见的阴离子间隙增高的代谢性酸中毒,可出现阴离子间隙和渗透压阶差的双重增高,但国内鲜有报道。本文收集92例伴有意识障碍的急性酒精中毒患者,其中阴离子间隙和渗透压阶差双重增高患者12例,对其进行治疗前后对比并分析,探讨其发生机制。     

早产儿转运中血气分析监测和处理对早产儿临床意义及影响

目的：探讨早产儿转运中的血气分析监测和处理对早产儿代谢性酸中毒的影响。方法回顾性分析转运途中未进行血气分析监测和处理患儿36例（对照组）与转运途中血气分析监测和处理患儿30例（观察组）。比较两组患儿在转运中代谢性酸中毒的发生率,入院后代谢性酸中毒的发生率,血气分析恢复到正常的时间和相关临床症状消失时间。结果对照组患儿入院后代谢性酸中毒发生率30.5%,观察组发生率40%;入院后监测血气分析,代谢性酸中毒的发生率分别是30.5%和13.3%。对照组代谢性酸中毒恢复正常时间（2.5±1.2）d,观察组恢复正常时间（1.7±1.1）d,差异有统计学意义（P<0.05）。结论早产儿转运中代谢性酸中毒发生率较高,监测和处理有助于降低早产儿代谢性酸中毒的发生率,及早维持患儿血气分析在正常范围内,为下一步救治提供条件。     

重症糖尿病酮症酸中毒患者的临床急诊急救

目的探讨重症糖尿病酮症酸中毒患者的临床急诊急救效果。方法将新疆维吾尔自治区人民医院及新疆医科大学第二附属医院2015年1月至2016年10月收治的100例重症糖尿病酮症酸中毒患者作为研究对象,采用随机法分成试验组与对照组,各50例,对照组使用胰岛素静脉持续滴注方法治疗,试验组采用胰岛素泵持续皮下注射法,在胰岛素治疗基础上,2组患者均进行补液、矫正电解质紊乱及矫正酸中毒治疗。对比分析2组患者治疗效果及不良反应发生率。结果对照组患者治疗总有效率为90.0%,试验组患者治疗总有效率为94.0%,2组患者总有效率差异无统计学意义(P>0.05);对照组低血糖发生率为26.0%,试验组为4.0%,试验组显著低于对照组,差异有统计学意义(P<0.05)。结论重症糖尿病酮症酸中毒患者应及早有效地诊断治疗,胰岛素、补液、矫正电解质紊乱及矫正酸中毒治疗效果较好,而且使用胰岛素泵持续皮下注射治疗能显著降低患者发生低血糖的几率。     

Metabolic acidosis not due to lactic acidosis in patients with severe acute asthma

Asthmatics seeking emergency care for severe acute asthma may show metabolic acidosis. We sought to determine the frequency of metabolic acidosis in such patients and to assess the relative contributions of renal bicarbonate loss and lactic acid accumulation to this acidosis. Twenty-two asthmatics (21-71 yr; four males, and 18 females) who came consecutively to the emergency department with severe acute asthma were studied. Most patients reported that their asthmatic symptoms had begun to worsen greater than or equal to 2 days before the emergency department visit. Within several hours, simultaneous measurements of arterial blood gases, whole blood lactate, and serum electrolytes were made. Ten of 22 patients were found to have metabolic acidosis (base deficit greater than 2 mEq/L). All ten patients had nonanion gap acidosis, while nine of ten had whole blood lactate values in the normal range (0.33 to 2.55 mmol/L). In the one patient with an elevated whole blood lactate level, the concentration of lactate in excess of normal (0.45 mmol/L) could not account for the magnitude of the base deficit (-4.9 mEq/L). We conclude that a) nonanion gap metabolic acidosis is very common in asthmatics with acute severe asthma (prevalence 45% in our series), and b) the mechanism of the base deficit in these patients is excessive renal bicarbonate excretion. We believe that the latter occurs as a renal compensatory response to a preceding period of hypocapnia due to hyperventilation related to worsening asthma.     

酒精性酮症酸中毒的诊疗进展

酒精性酮症酸中毒（alcoholic ketoacidosis,AKA）是指患者在大量饮酒后发生严重呕吐、中断饮食或其他伴发病,从而引起脱水、酮症酸中毒,属代谢系统急症之一。酒精性酮症酸中毒由美国Dillon等于1940年首次提出。酒精中毒患者中大约有10%表现为酒精性酮症酸中毒,多见于肝病和酗酒者,为慢性酒精中毒死亡的主要原因之一。     

依托型急救中心急性中毒流行病学与急救特点分析

目的 研究依托型急救中心急诊内科收治急性中毒患者的流行病学与急救特点.方法 采用回顾性研究方法,对2004-2009年在福建省急救中心内科就诊的各类急性中毒患者的性别、年龄、中毒原因、种类、毒物名称、入侵途径、急诊诊断、急救处置、去向及转归等,进行登记并分析.结果 共收治急性中毒患者2867例,男女比例为1∶1.04,平均33.8岁,其中18～40岁年龄组占76.39%.所有中毒例数以1月份最多,占全部11.33%;中毒类别位居前四位的依次是酒精中毒(54.55%),药物中毒(25.95%),农药中毒(5.65%),毒品中毒(4.88%);毒品中毒大部分为年龄≤25岁(56.44%),平均年龄为28.2岁,明显低于药物中毒和酒精中毒(P＜0.01);69.54%患者经急救处理后离院随诊观察,需要住院者占30.39%,仅4例发生死亡.结论 城市急性中毒以酒精和药物为著;依托型急救中心模式中"院前急救-急诊科-院内救治"的急救绿色通道,对于提高急性中毒的抢救成功率和成活率具有重要意义.     

急性农药中毒患者的临床特征及预后影响因素分析

目的分析急性农药中毒患者的临床特征及预后影响因素。方法纳入我院收治的417例急性农药中毒患者,根据随访6个月内是否死亡分为存活组(370例)和死亡组(47例)。比较两组的临床特征、临床资料,分析影响急性农药中毒患者预后的危险因素。结果存活组的中枢神经系统症状、循环系统症状、呼吸系统症状发生率均显著低于死亡组(P<0.05);死亡组与存活组的中毒途径有显著差异(P<0.05)。院前时间、APACHEⅡ评分、农药剂量、院前急救率、农药类型、ChE、β-内啡肽、和肽素水平均为影响急性农药中毒患者预后的独立因素(P<0.05)。结论临床中对于急性农药中毒患者,应及时开展急救,并针对影响预后的独立因素及时开展对症治疗,以促进患者预后的改善。     

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.     

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.     

血液净化救治急性重症中毒并急性肾功能衰竭30例的临床分析

目的：总结急性重症中毒并急性肾功能衰竭（ARF）的临床特点并探讨多种血液净化（BP）模式抢救急性重症中毒的临床疗效。方法：回顾性分析我院30例急性中毒并ARF患者,其中9例行血液透析（HD）治疗,11例行HD串联血液灌流（HD＋HP）治疗,10例采用连续性静脉-静脉血液透析滤过（CVVHDF）治疗,各组均给予综合性治疗,比较单纯HD组、HD＋HP组、CVVHDF组之间治疗效果。结果：CVVHDF组治愈率高,肾功能恢复优于其他血液净化组（P〈0．05）,昏迷者的清醒时间快,住院时间缩短（P〈0．05）,无明显毒副作用。结论：CVVHDF、HD＋HP血液净化治疗抢救各种急性中毒并ARF患者成功率高,对急性重症中毒伴多器官功能障碍者,提倡早期行CV—VHDF治疗,同时重视洗胃、营养支持、水电解质酸碱平衡、抗感染等综合治疗,以利于急危重症中毒患者的救治。     

注射用复合辅酶对急性酒精中毒所致心肌损伤的治疗研究

目的探讨复合辅酶对急性酒精中毒所致心肌损伤的保护作用。方法选取近三年急诊收治的急性酒精中毒患者中有心肌损伤者204例,随机分为对照组和研究组各102例。分别给予常规治疗和加用复合辅酶治疗,比较两组治疗前后心电图、心肌酶谱的变化。结果各指标治疗前组间比较均无明显差异,治疗后组间比较：AST无显著差异,研究组心电图、LDH、CK、CK-MB均显著降低;各指标治疗前后组内比较均有显著改善。结论复合辅酶可有效改善急性酒精中毒患者的心肌损伤。     

Pathogenic mechanism, prophylaxis, and therapy of symptomatic acidosis induced by acetazolamide.

BACKGROUND: Acetazolamide, a noncompetitive carbonic anhydrase inhibitor, can produce symptomatic acidosis and bone marrow suppression by a mechanism that is still unknown. This presentation occurs in the elderly, patients with renal or liver failure, people with diabetes, and newborns. The objective of this study was to understand the pathogenic mechanism of these adverse effects and to propose a possible prophylaxis and therapy. METHODS: Four human clinical cases were studied, and one animal experiment was performed. Four preterm newborns with posthemorrhagic ventricular dilation developed severe metabolic acidosis after treatment with acetazolamide. The acidosis suddenly disappeared after a packed red blood cell transfusion. Metabolic studies were performed in one patient and in newborn guinea pigs treated with 200 mg/kg acetazolamide. RESULTS: Acetazolamide can produce severe lactic acidosis with an increased lactate-to-pyruvate ratio, ketosis with a low beta-hydroxybutyrate-to-acetoacetate ratio, and a urinary organic acid profile typical of pyruvate carboxylase deficiency. The acquired enzymatic injury resulting from the inhibition of mitochondrial carbonic anhydrase V that provides bicarbonate to pyruvate carboxylase can produce tricarboxylic acid cycle damage. We demonstrate that the dramatic disappearance of metabolic acidosis and normalizing metabolism after blood transfusion were due to the citrate contained in the packed red blood cell bag. This hypothesis was confirmed by animal experimentation. We argue that the metabolic disorder and bone marrow suppression may be related. CONCLUSION: We demonstrate how acetazolamide can lead to symptomatic metabolic acidosis and probably to bone marrow suppression. We suggest citrate as a possible prophylaxis and treatment for these adverse reactions.     

Survival from profound alcohol-related lactic acidosis.

We present the case of a patient with profound alcohol-related lactic acidosis (lactate = 16.1 mmol/L; pH = 6.67) associated with a multitude of metabolic derangements who made a remarkable recovery following aggressive management. The patient was in extremis upon arrival in the emergency department (ED), and resuscitation was begun immediately. While in the ED, the problem list generated included: acute alcohol intoxication, severe lactic acidosis, dehydration, hypothermia, hypoglycemia, acute renal insufficiency, and hepatic failure. Resuscitation continued in the intensive care unit with remarkable improvement and satisfactory outcome. In this patient, the severe lactic acidosis and associated abnormalities were all attributed to acute and chronic effects of ethanol. A brief summary of the proposed mechanism by which these metabolic derangements developed and an outline of her management follows.