Myocardial infarction after acute carbon monoxide poisoning: case report

A 28-year-old man with acute myocardial infarction after carbon monoxide poisoning is reported. He had chest pain after the exposure to carbon monoxide. The electrocardiogram, serum enzymes, and technetium-99m pyrophosphate scintigrams showed anterior myocardial infarction. The coronary angiogram, which was performed one month after the onset, showed no visible atherosclerotic lesion. As to the cause of myocardial infarction, it is assumed that carbon monoxide reduced the oxygen supply to the myocardium and might induce coronary artery spasm with or without accompanying coronary thrombosis.     

校正的QT间期延长在一氧化碳中毒相关迟发性神经精神后遗症中的预测价值

目的 探讨心电图校正的QT间期（QTc）延长对一氧化碳（CO）中毒患者发生迟发性神经精神后遗症（DNS）的预测价值。方法 回顾性分析223例CO中毒患者的临床资料,根据有无DNS分为DNS组（31例）和非DNS组（202例）。采用单因素及多因素logistic回归分析确定影响DNS发生的独立危险因素,采用受试者工作特征（ROC）曲线分析QTc检测时间对DNS的预测价值。结果 233例CO中毒患者中有31例（13.3%）发生DNS,单因素logistic分析结果显示,格拉斯哥昏迷评分（GCS）<9分、短暂意识丧失、CO暴露到入院时间延长、QTc延长等与DNS发生相关（P<0.05）。多因素logistic回归分析结果显示,GCS<9分、CO暴露到入院时间>6h和QTc延长是DNS发生的独立危险因素（P<0.05）。ROC曲线分析结果显示,在CO暴露<2h、2～4h、4～6h进行QTc检测对DNS的发生均具有较高的预测价值,并且在CO暴露6h内检测QTc对DNS的预测价值最高。结论 在CO暴露6h内通过心电图检查发现QTc延长是预测CO中毒后发生DNS的新预测指标。     

Delayed neuropathology after carbon monoxide poisoning is immune-mediated

The neuropathological sequelae of carbon monoxide (CO) poisoning cannot be explained by hypoxic stress alone. CO poisoning also causes adduct formation between myelin basic protein (MBP) and malonylaldehyde, a reactive product of lipid peroxidation, resulting in an immunological cascade. MBP loses its normal cationic characteristics, and antibody recognition of MBP is altered. Immunohistochemical evidence of degraded MBP occurs in brain over days, along with influx of macrophages and CD-4 lymphocytes. Lymphocytes from CO-poisoned rats subsequently exhibit an auto-reactive proliferative response to MBP, and there is a significant increase in the number of activated microglia in brain. Rats rendered immunologically tolerant to MBP before CO poisoning exhibit acute biochemical changes in MBP but no lymphocyte proliferative response or brain microglial activation. CO poisoning causes a decrement in learning that is not observed in immunologically tolerant rats. These results demonstrate that delayed CO-mediated neuropathology is linked to an adaptive immunological response to chemically modified MBP.     

Echocardiographic findings after acute carbon monoxide poisoning.

Myocardial lesions are frequently seen at necropsy after fatal carbon monoxide poisoning. Clinically, while there have been numerous reports of chest pain and electrocardiographic changes associated with acute carbon monoxide poisoning, other evidence for left ventricular abnormality has not been reported. The echocardiographic findings in five cases of non-fatal poisoning are presented here. Abnormal left ventricular wall motion was shown by echocardiography in 3 cases. Motion returned to normal in 2 of the 3 in follow-up tracings. Echocardiograms on 3 of the 5 patients showed mitral valve prolapse. Though the mitral valve prolapse may have been present before the poisoning, the reported high incidence of papillary muscle lesions in fatal cases suggests a possible relation of the prolapse to the effects of the carbon monoxide poisoning.     

广西急性一氧化碳中毒后迟发性脑病的预后因素分析

目的收集广西部分医院急性一氧化碳中毒后迟发性脑病(DEACMP)患者的临床资料,分析影响DEACMP预后的因素。方法回顾分析2008~2014年广西武鸣县人民医院、广西区人民医院、广西区江滨医院住院的52例DEACMP患者的临床资料,病后3个月根据患者日常生活能力量表(ADL)的评分结果分为无效组25例和好转组27例,分别比较两组患者性别、年龄、基础疾病、暴露在CO中的时间、昏迷时间、假愈期、急性期是否高压氧(HBO)治疗、并发症、早期头颅CT、MRI是否异常、入院时心肌酶谱、心电图、血白细胞总数是否异常、入院时ADL评分以及是否使用依达拉奉15项可能影响DEACMP预后的因素。结果年龄、暴露在CO中的时间、假愈期、急性期是否行HBO治疗、并发症、早期头颅MRI是否异常、入院时ADL评分与DEACMP患者预后相关(P0.05),其中年龄、暴露在CO中的时间、入院时ADL评分意义更大(P0.01),而其余因素对DEACMP患者预后无明显影响(P0.05)。结论年龄较大、暴露在CO中的时间长、假愈期较短、急性期未行HBO治疗、早期头颅MRI异常、并发症以及入院时ADL评分较低均提示DEACMP患者预后差,应高度警惕。     

Value of early-stage cerebral oxygen utilization coefficient in predicting delayed encephalopathy after acute carbon monoxide poisoning

正Objective To investigate the dynamic change in cerebral oxygen utilization coefficient(O2UCc)in the early stage of acute severe carbon monoxide poisoning(ASCMP)and its value in predicting delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Methods A prospective observational study was conducted for patients with ASCMP who were admitted to our hospital from November 2013 to March 2016,and their     

Myocardial infarction after carbon monoxide exposure--a case report

We present the case of a patient with the myocardial infarction as the result of carbon monoxide poisoning. We consider that a careful electrocardiographic and enzymatic monitoring of all patients after CO exposure is important for early diagnosis and treatment of myocardial infarction, especially because the patients often do not complain of any chest pain and ischaemic features in an electrocardiogram are withdrawing rather fast.     

急性一氧化碳中毒迟发性脑病的临床表现及预后相关因素

目的通过对15例急性一氧化碳中毒迟发性脑病的临床资料分析,探讨其发病及预后的相关因素。方法回顾性分析我院2006年6月~2014年1月收治的一氧化碳中毒迟发性脑病15例患者的临床资料,根据临床表现分为轻度、中度和重度。结果患者临床主要表现为智能下降、精神行为异常,肌张力增高、震颤、运动障碍等帕金森样症状。头颅CT或MRI检查示,双侧额叶、皮质下脑白质,侧脑室旁脑白质及基底节区对称性低密度、长T1、长T2及脱髓鞘改变。脑电图有不同程度的慢波改变。一氧化碳暴露时间≥4h的5例中,3例重度,2例中度;暴露时间<4h的10例中,中度5例,轻度5例。有脑血管病危险因素的7例中,3例重度,4例中度。经高压氧等综合治疗,1例85岁重度患者无效,14例临床症状均有不同程度改善。轻度5例中,痊愈4例、好转1例;中度7例均好转;重度3例中,好转2例、无效1例。结论一氧化碳中毒迟发性脑病患者大脑皮质和基底节区神经功能损害明显。高压氧等综合治疗可改善预后。年龄越大、病情越重,预后越差。     

Cutaneous blisters and carbon monoxide poisoning

We present the cases of three patients with skin blisters following carbon monoxide (CO) poisoning. Their blisters appeared to be related to the severity of the poisoning (HbCO levels of more than 40%). Two of the three patients died despite aggressive initial 100% surface oxygen followed by hyperbaric oxygen therapy. The pathophysiology of this type of blister remains unresolved. It could result from pressure necrosis alone or from a combination of pressure necrosis and direct CO inhibition of tissue oxidative enzymes. Although skin involvement as a result of CO poisoning is less frequently reported today than in the past (perhaps because of misidentified burns or because of more aggressive resuscitation and treatment protocols), the physician should recognize that such blisters may signal severe CO poisoning.     

Effects of Ginaton on nitric oxide and nitric oxide synthase in patients with delayed encephalopathy after carbon monoxide poisoning

正Objective To observe the effects of Ginaton on blood nitric oxide(NO)and nitric oxide synthase(NOS)in patients with delayed encephalopathy after acute carbon monoxide poisoning(DEACMP).Methods A total of116 patients with DEACMP who were treated in Emergency Department of Harrison International Peace Hospi-     

The investigation of ischemic myocardial damage in patients with carbon monoxide poisoning]

OBJECTIVE: Poisoning with carbon monoxide (CO) due to flash gas heater or stove being an important health problem in our region, causes significant pathologies in the body as well as death by decreasing oxygen-carrying capacity of blood. This study was planned to assess whether or not myocardial damage occurs in patients with CO poisoning. METHODS: Forty consecutive adult patients with CO poisoning (30 females and 10 males) were included in this study. The mean age of the patients was 28.5+/-9.9 years (range: 15-56). The demographic characteristics, vital signs, the origin of CO gas, risk factors for coronary artery disease (CAD) and smoking habit of the patients were recorded. The evaluation of Glasgow Coma Scale score, electrocardiogram (ECG), peripheral arterial blood gases, complete blood count, creatine kinase (CK), creatine kinase-myocardial band (CKMB), troponin-T measurements were performed in all cases. Additionally, myocardial perfusion SPECT was performed in three cases with carboxyhemoglobin (COHb) levels over 50%. RESULTS: Sinus tachycardia, was observed in 9 cases. Ventricular bigeminy was seen in a case with troponin-T positive test. Six of 40 cases (15%) had significantly increased CK and CK-MB levels with normal troponin-T measurements. High troponin-T levels (0.13 ng/ml) were detected only in 1 case with COHb level of 61.3%. Myocardial SPECT was performed in 3 cases with COHb levels higher than 50% and no images compatible with defects could be identified. CONCLUSION: The results suggested that significant myocardial damage and life-threatening cardiac hemodynamic changes do not develop in CO-poisoned patients with COHb level below 60 % and without any known underlying CAD. It is not necessary to routinely measure CK, CK-MB and troponin-T, and perform myocardial perfusion SPECT in acute CO poisoning cases without any ECG abnormality, ischemic cardiac symptoms or known CAD.     

Subacute sequelae of carbon monoxide poisoning

From January 1980 to August 1983, 213 patients with carbon monoxide poisoning were seen; 131 received hyperbaric oxygen and had no sequelae. Eighty-two patients were treated with normobaric oxygen; ten (12.1%) returned with clinically significant sequelae. The specific neurological sequelae included headaches, irritability, personality changes, confusion, and loss of memory. This recurrent symptomatology developed within one to 21 days (mean, 5.7 days) after the initial exposure, although no reexposure occurred. These recurring symptoms resolved rapidly with hyperbaric oxygen therapy. We recommend that hyperbaric oxygen therapy be used whenever CO poisoning symptoms recur.     

Cardiovascular effects of carbon monoxide poisoning

Carbon monoxide (CO) poisoning is an important health problem. Cardiac abnormalities may occur in patients with CO poisoning; however, the severity and duration of cardiac abnormalities are not well known. In this study, cardiac structures and function in CO poisoning were evaluated prospectively. Twenty patients were enrolled in the study. Echocardiographic examination was performed in all patients on admission, at 24 hours, and within the first week. B-type natriuretic peptide and carboxyhemoglobin levels were measured. Patients with increased cardiac markers underwent coronary angiography. Cardiac markers were high in 6 patients. Patients with high cardiac markers had significantly higher carboxyhemoglobin levels and longer exposure to CO. Left ventricular ejection fraction (LVEF) was <45% in 8 patients (group I) on admission and >55% in 7 patients in group I 24 hours after echocardiography. A significant negative correlation was found between B-type natriuretic peptide and LVEF on admission (r = -0.586, p <0.01). The decrease in LVEF was also negatively correlated with carboxyhemoglobin level and CO exposure duration. All angiograms showed normal coronary arteries. In conclusion, despite normal coronary arteries, myocardial dysfunction may occur in patients with CO poisoning. LV systolic function might be normal or mildly to severely impaired. However, most of the myocardial dysfunction dissipates at 24 hours in patients with CO poisoning.