Unusual complication of aluminum phosphide poisoning: Development of hemolysis and methemoglobinemia and its successful treatment

Methemoglobinemia and hemolysis are rare findings following phosphine poisoning. In this paper, a case of aluminum phosphide (AlP) poisoning complicated by methemoglobinemia and hemolysis with a successful treatment is reported. A 28-year-old male patient presented following intentional ingestion of an AlP tablet. In this case, hematuria, hemolysis and methemoglobinemia were significant events. A methemoglobin level of 46% was detected by CO-oximetry. The patient was treated with ascorbic acid and methylene blue and he also received supportive care. Two weeks after admission, the patient was discharged from the hospital. Hemolysis and methemoglobinemia may complicate the course of phosphine poisoning.     

Aluminum phosphide poisoning: Possible role of supportive measures in the absence of specific antidote

Aluminum phosphide (ALP) poisoning is one of the major causes of suicidal deaths. Toxicity by ALP is caused by the liberation of phosphine gas, which rapidly causes cell hypoxia due to inhibition of oxidative phosphorylation, leading to circulatory failure. Treatment of ALP toxicity is mainly supportive as there is no specific antidote. We recently managed 7 cases of ALP poisoning with severe hemodynamic effects. Patients were treated with supportive measures including gastric lavage with diluted potassium permanganate, coconut oil and sodium-bicarbonate first person account should be avoided in a scientific paper. Intravenous magnesium sulfate, proper hemodynamic monitoring and vasopressors. Four out of 7 survived thus suggesting a role of such supportive measures in the absence of specific antidote for ALP poisoning.     

Severe myocardial depression in a patient with aluminium phosphide poisoning: A clinical, electrocardiographical and histopathological correlation

Aluminium phosphide poisoning is very common in India. It is one of the most fatal poisons. The clinical spectrum of poisoning varies depending upon the dosage and duration of consumption. The main effect of the poison is due to the release of phosphine which inhibits cytochrome oxidase and thereby hampers cellular oxygen utilization. Almost any organ can be affected by aluminium phosphide poisoning. We report a case where the heart was the predominantly affected organ. We describe the clinical symptoms and signs and their correlation with electrocardiographic and histopathological examinations.     

Successful management of aluminium phosphide poisoning using intravenous lipid emulsion: Report of two cases

Aluminum phosphide (ALP) is a cheap, easily available agricultural pesticide which causes lethal poisoning by liberation of phosphine and inhibition of cytochrome c oxidase thereby leading to cellular hypoxia. Although there is no known specific antidote, clinical trials are still going on. We present here two cases of ALP poisoning who were successfully managed by treatment with lipid emulsion and intravenous magnesium sulfate.     

Oxidative stress determined through the levels of antioxidant enzymes and the effect of N-acetylcysteine in aluminum phosphide poisoning

Introduction:

The primary objective of this study was to determine the serum level of antioxidant enzymes and to correlate them with outcome in patients of aluminum phosphide (ALP) poisoning and, secondly, to evaluate the effect of N-acetylcysteine (NAC) given along with supportive treatment of ALP poisoning.

Design:

We conducted a cohort study in patients of ALP poisoning hospitalized at a tertiary care center of North India. The treatment group and control group were enrolled during the study period of 1 year from May 2011 to April 2012.

Interventions:

Oxidative stress was evaluated in each subject by estimating the serum levels of the enzymes, viz. catalase, superoxide dismutase (SOD) and glutathione reductase (GR). The treatment group comprised of patients who were given NAC in addition to supportive treatment (magnesium sulfate and vasopressors, if required), while in the control group, only supportive treatment was instituted. The primary endpoint of the study was the survival of the patients.

Measurements and Results:

The baseline catalase (P = 0.008) and SOD (P < 0.01) levels were higher among survivors than non-survivors. Of the total patients in the study, 31 (67.4%) expired and 15 (32.6%) survived. Among those who expired, the mean duration of survival was 2.92 ± 0.40 days in the test group and 1.82 ± 0.33 days in the control group (P = 0.043).

Conclusions:

This study suggests that the baseline level of catalase and SOD have reduced in ALP poisoning, but baseline GR level has not suppressed but is rather increasing with due time, and more so in the treatment group. NAC along with supportive treatment may have improved survival in ALP poisoning.     

Depmas双重血液净化的疗效观察

目的 观察Depmas双重血液净化系统治疗急性重度有机磷农药中毒的临床疗效.方法 选取急性重度有机磷农药中毒患者147例,分为4组,常规治疗组只行药物治疗;血液灌流组在常规治疗基础上联用HA230树脂血液灌流器行血液灌流治疗;血液灌流联合血浆置换组在常规治疗基础上联用HA230树脂血液灌流器行血液灌流及百特血滤机行血浆置换治疗;Depmas组在常规治疗基础上通过百特血滤机进行血浆分离,再对分离的血浆串联HA230树脂血液灌流器及BS330血浆胆红素吸附器行血液灌流治疗.观察4组患者的存活率,死亡患者的平均存活时间,外周血中胆碱酯酶及胆红素浓度的变化.结果 血液灌流组、血液灌流联合血浆置换组及Depmas组较常规治疗组患者存活率升高,死亡患者的平均存活时间延长,外周血中的胆碱酯酶浓度升高、胆红素浓度降低,差异均具有统计学意义（P＜0.01）;血液灌流联合血浆置换组及Depmas组较血液灌流组患者存活率升高,死亡患者的平均存活时间延长,外周血中胆碱酯酶浓度升高、胆红素浓度降低,差异亦具有统计学意义（P＜0.05）;血液灌流联合血浆置换组与Depmas组患者存活率、死亡患者的平均存活时间、外周血中胆碱酯酶和胆红素浓度差异均无统计学意义（P＞0.05）.结论 Depmas双重血液净化系统治疗急性重度有机磷农药中毒疗效显著.     

人脐血单个核细胞移植治疗急性一氧化碳中毒后迟发脑病1年随访

背景：研究报道在特定的体内外环境下,脐血间充质干细胞能够诱导分化成为包括神经干细胞在内的多种组织细胞。 目的：评价人脐血单个核细胞经腰穿途径移植后治疗急性一氧化碳中毒后迟发性脑病的疗效及安全性。 方法：一氧化碳中毒后迟发性脑病患者60例随机分为2组。对照组给予高压氧及药物治疗;治疗组采用鞘内注射法将经密度梯度离心法分离出的人脐血单个核细胞移植到一氧化碳中毒性脑病患者的蛛网膜下腔,余治疗方法同对照组。分别于人脐血单个核细胞移植前、移植后3,9,12个月对患者进行简易精神状态检查法、改良Asworth肌肉痉挛程度分级及日常生活量表评分检查;比较两组患者MRI变化;同时对随诊患者行胸片、心电图及血生化检查,客观评价人脐血单个核细胞移植的安全性。 结果与结论：人脐血单个核细胞移植3,9,12个月,治疗组Asworth肌肉痉挛程度分级评分均显著低于对照组(P=0.032);移植后9,12个月简易智力状况检查法及日常生活量表评分均显著高于对照组(P < 0.05);两组患者神经功能在各时间点的变化趋势相似。人脐血单个核细胞移植后12个月MRI检查结果显示,治疗组患者MRI改善程度较对照组明显。提示鞘内注射移植人脐血单个核细胞治疗一氧化碳中毒后迟发脑病疗效优于高压氧治疗。中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程全文链接：     

慢性砷中毒对小鼠海马CA1区星形胶质细胞的影响

目的观察慢性砷中毒对成年小鼠海马CA1区星形胶质细胞的影响,探讨慢性砷中毒对成年小鼠脑部的神经毒性。方法选取健康成年昆明小鼠60只,雌雄各半,分为对照组、慢性砷中毒组,每组30只,分别以蒸馏水、1/10 LD50As2O3即As2O34.5 mg·kg^4.d^-1灌胃,连续3个月,根据其体重变化随时调整用药剂量。灌胃结束后,采用Y型电迷宫检测各组小鼠学习与记忆的功能,其后取小鼠海马组织,利用免疫组织化学技术检测砷中毒对小鼠海马CA1区胶质原纤维酸性蛋白（GFAP）表达的影响。结果与正常对照组比较,砷中毒组小鼠的学习、记忆能力明显低于对照组（P〈0.05）;免疫组化染色显示小鼠海马CA1区GFAP阳性细胞明显增多（P〈0.05）,阳性反应产物平均光密度增高（P〈0.05）。结论慢性砷中毒可引起小鼠海马CA1区星形胶质细胞反应性增生。     

体外膜氧合法对急性一氧化碳中毒家兔的治疗效应

目的:观察臭氧体外循环膜氧合治疗(ECMO3)对急性一氧化碳中毒(ACOP)家兔的效果,并探讨其在ACOP治疗中的疗效和安全性。方法:32只新西兰白兔单次腹腔注射99.99%CO(200mL/kg)建模,随机分为ECMO3组(ECMO3组)、面罩吸氧治疗组(FIO2组)、未给予干预措施的ACOP组(ACOP组)和对照组(control组)。动态监测实验兔的碳氧血红蛋白(COHb)浓度、血氧饱和度(SO2)、全血剩余碱(BE-B)的变化以及动物生命体征的变化。结果:3组实验兔于建模30min后COHb值显著升高(P0.01),并出现中毒反应。经ECMO3和FIO2治疗后,实验兔的呼吸和心率得到纠正,并明显慢于ACOP组(P0.01)。经ECMO3治疗后,ECMO3组的COHb值明显低于FIO2组及ACOP组(F=42.799,P0.01);于治疗0.5h后,ECMO3组和FIO2组的SO2和BE-B与ACOP组比较明显升高(P0.05,P0.01)。结论:ECMO3能够有效降低COHb浓度、提高SO2,纠正酸中毒,且安全性好,为一氧化碳中毒的治疗提供了一种新的尝试。     

Effect of hypotensive agents on baroreceptor reflexes in waking animals

The effect of -methyldopa, clonidine, pentobarbital sodium, and reserpine on reflex bradycardia induced by an artificial rise of the systemic arterial pressure (BP) was studied in experiments on waking cats. The substances used, which have a tranquilizing action, led to various changes in function of the baroreceptor reflexes, the initial BP level, and the cardiac frequency.Department of Experimental Physiology and Pharmacology, Central Research Laboratory, Academician I. P. Pavlov First Leningrad Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR V. N. Chernigovskii). Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 87, No. 2, pp. 166–168, February, 1979.     

Effect of 4-aminopyridine on development of experimental botulinum poisoning

Bulletin of Experimental Biology and Medicine -     

高氧液对大鼠急性一氧化碳中毒脑损伤保护作用的研究

目的:探讨不同剂量高氧液(hyperoxygenated solution,HOS)对急性CO中毒脑损伤的保护作用,为临床应用提供实验依据。方法:将30只SD大鼠随机分为5组,每组6只。正常组(N组)、中毒组(C组)和中毒治疗组(H组),H组再根据输注HOS剂量不同分为,HOS 10 ml/kg(H10组)、15 ml/kg(H15组)和20 ml/kg(H20组)。C组与H组大鼠经腹腔注入CO 120 ml/kg建立中毒模型,N组给予等量空气。各组大鼠分别在输注不同剂量的液体后即刻取血0.5 ml行血气检测,1 d抽取血3 ml进行神经元特异性敏感生化指标测定。实验结束后,所有动物均在麻醉状态下切取部分脑组织制作病理切片行病理学观察。结果:CO 120 ml/kg腹腔注射1.5 h能引起严重的低氧血症。中毒后1 d神经元特异性烯醇化酶、S-100β蛋白明显升高(P0.01)。中毒后24 h脑细胞出现明显水肿、间质增宽。中毒治疗组在静脉输注不同剂量的HOS后,动脉血氧分压(mm Hg)由43.04±4.13分别上升到69.56±3.41、77.11±2.49和81.65±3.85,脑组织病理学改变明显减轻,其中H20组降低最明显,具有显著的剂量依赖性。结论:HOS能明显提高CO中毒大鼠的Pa O2和动脉血氧饱和度,降低神经元特异性敏感指标的含量,对一氧化碳中毒脑损伤具有很好的保护作用,并具有剂量依赖关系。     

Effect of chronic metabolic acidosis on ammonia production fromL-glutamine in microdissected rat nephron segments

To evaluate the role of each nephron segment in renal ammoniagenesis, distribution of renal ammoniagenic activity along the nephron in control and acidotic rats was examined. We used our original aerobic incubation system and ammonia produced from glutamine in 7 defined segments of microdissected nephron was measured using the enzymatic cycling method.When ammonia production in the control was compared in each nephron segment, the highest specific activity of ammoniagenesis per mm tubular length and that per g protein were observed in the proximal straight tubule (PST) and the thick ascending limb of Henle's loop, respectively. Chronic metabolic acidosis increased ammonia production per mm tubular length markedly in the proximal convoluted tubule (PCT) (+171%), moderately in the medullary collecting tubule (+123%) and PST (+77%), and slightly in the distal convoluted tubule (+52%), revealing that the highest activity of ammoniagenesis was located in PCT and PST in acidosis.These data indicate that proximal tubules have major roles in renal ammoniagenesis both in the control and in acidosis. From the early observation of glutaminase I isoenzyme distribution along the nephron, our data suggest that not only phosphate-dependent glutaminase but also phosphate-independent glutaminase may have important roles in renal ammoniagenesis.This study was presented in part at 26th Congress of Japanese Society of Nephrology, Kyoto, 1983     

Effect of acute metabolic acidosis on transmembrane electrolyte gradients in individual renal tubule cells

We studied the effect of acute metabolic acidosis on potassium, sodium and chloride gradients across the apical membrane of proximal and distal tubule cells by determining electrolyte concentrations in individual cells and in tubule fluid employing electron microprobe analysis. Cellular measurements were performed on freeze-dried cryosections of the renal cortex, analysis of tubule fluid electrolyte concentrations on freeze-dried microdroplets of micropuncture samples obtained from proximal and from early and late distal collection sites. Acidosis (NH₄Cl i.v. and i.g.) induced a substantial rise in plasma potassium concentration without significant effects on cell potassium concentrations. Potassium concentrations along the surface distal tubule were also unaltered; thus the chemical driving force for potassium exit from cell to lumen was not affected by acidosis. In all but intercalated cells acidosis markedly increased cell phosphorus concentration and cell dry weight indicating cell shrinkage and thus diminution of cell potassium content. Because the increase in intracellular chloride concentration exceeded the increase in plasma chloride concentration, the chemical chloride gradient across the contraluminal membrane was markedly depressed by acidosis.     

Effect of arm-cranking on leg blood flow and noradrenaline spillover during leg exercise in man

Controversy exists whether recruitment of a large muscle mass in dynamic exercise may outstrip the pumping capacity of the heart and require neurogenic vasoconstriction in exercising muscle to prevent a fall in arterial blood pressure. To elucidate this question, seven healthy young men cycled for 70 minutes at a work load of 5540%VO_2max. At 30 to 50 minutes, arm cranking was added and total work load increased to (mean ± SE) 82 ± 4% of Vo_2max. During leg exercise, leg blood flow average 6.15 4.511 minutes^-1, mean arterial blood pressure 137 ± 4 mmHg and leg conductance 42.3 ± 2.2 ml minutes^-1 mmHg^-1. When arm cranking was added to leg cycling, leg blood flow did not change significantly, mean arterial blood pressure increased transiently to 147 ± 5 mmHg and leg vascular conductance decreased transiently to 33.5 ± 3.1 ml minutes^-1 mmHg^-1. Furthermore, arm cranking doubled leg noradrenaline spillover. When arm cranking was discontinued and leg cycling continued, leg blood flow was unchanged but mean arterial blood pressure decreased to values significantly below those measured in the first leg exercise period. Furthermore, leg vascular conductance increased transiently, and noradrenaline spillover decreased towards values measured during the first leg exercise period. It is concluded that addition of arm cranking to leg cycling increases leg noradrenaline spillover and decreases leg vascular conductance but leg blood flow remains unchanged because of a simultaneous increase in mean arterial blood pressure. The decrease in leg vascular conductance observed when arm cranking increased mean arterial blood pressure could be regarded more as a measure to prevent overperfusion than a measure to maintain arterial blood pressure.     

Effect of chronic hypoxia on pulmonary artery blood velocity in rats as assessed by electrocardiography-triggered three-dimensional time-resolved MR angiography

Pulmonary arterial hypertension (PAH) is a severe disease that leads to increased pulmonary vascular resistance and right heart failure. Noninvasive methods are needed to detect changes in the pulmonary artery circulation during PAH establishment and/or treatment. Pulmonary blood flow velocity can be evaluated by dynamic MR angiography, although the relevance of such data in the context of PAH remains to be demonstrated. A novel dynamic MR angiography technique was used in this work to measure blood flow velocity in the pulmonary arteries of the same living animals, before and after the establishment of chronic hypoxia‐induced PAH. Chronic hypoxia decreased significantly the blood flow velocity (43.8 ± 4.9 vs 24.3 ± 8.7 cm/s) on electrocardiography‐triggered time‐resolved angiograms. In parallel, chronic hypoxia‐induced PAH was confirmed from invasive measurements of the mean pulmonary arterial pressure (32.1 ± 4.8 vs 12.5 ± 2.2 mmHg) and the ratio of the right ventricle weight to the left ventricle plus septum weight (Fulton index: 0.54 ± 0.06 vs 0.27 ± 0.04). This study demonstrates the potential interest of dynamic MR angiography for the investigation of experimental models and for the evaluation of treatment efficacy. Copyright © 2010 John Wiley & Sons, Ltd.