Early Stage Blood Purification for Paraquat Poisoning: A Multicenter Retrospective Study.

OBJECTIVES: To evaluate the efficacy of conservative treatment vs. hemoperfusion (HP) vs. HP + continuous veno-venous hemofiltration (CVVH) for acute Paraquat (PQ) poisoning. METHODS: This was a multicenter retrospective study of patients with PQ poisoning between January 2013 and June 2014. Clinical data and PQ serum levels were collected at baseline and after 24, 48, and 72 h of treatment. RESULTS: Seventy-five, 65, and 43 underwent conservative treatment only (conservative treatment group), conservative treatment + HP (HP group), and conservative treatment + HP + CVVH (HP + CVVH group), respectively. PQ serum levels decreased in all groups after 72 h of treatment (p < 0.001); meanwhile, these values decreased faster in the HP and HP + CVVH groups compared with the conservative treatment group. More importantly, PQ blood levels were significantly lower in the HP + CVVH group compared with the HP group at 24 h (p < 0.05). Sequential organ failure assessment (ΔSOFA) values in the HP and HP + CVVH groups were significantly lower compared with that obtained for the conservative treatment group (p < 0.05). The 60-day survival rates were 21.3, 43.1 and 46.5%, respectively. Multivariate analysis indicated that age, PQ dose, admission PQ levels, and admission SOFA score were independently associated with mortality. HP and HP + CVVH were protective factors. CONCLUSION: Early HP or HP + CVVH after PQ poisoning could decrease PQ blood levels, alleviate organ damage, and increase survival.

[Rapid determination of 28 pesticides and tetramine in whole blood by online gel permeation chromatography coupled with gas chromatography-mass spectrometry].

OBJECTIVE: To study the influences of carbon disulfide (CS2) exposureon fatty acid metabolism in apolipoprotein E (ApoE) knockout mice and C57BL/6J mice. METHODS: Twenty-four male ApoE knockout mice were randomly and equally divided into four groups: a CS2-exposed normal diet group, a CS2-unexposed normal diet group, a CS2-exposed high-fat diet group, and a CS2-unexposed high-fat diet group. Twenty-four C57BL/6J male mice were divided into four groups in the same way. The CS2-exposed groups were exposed to CS2 (1 g/m³) by static inhalation for 5 hours a day, 5 days a week. After two weeks, the whole blood of mice was collected. Methyl ester derivatization of fatty acids was performed using an acid-catalyzed method. Fatty acid contents before and after exposure were compared by gas chromatography-mass spectroscopy. RESULTS: There were significant differences in fatty acid contents of mice between the four groups. For the C57BL/6J mice, the arachidic acid contents in the CS2-exposed high-fat diet group were significantly lower than those in the CS2-unexposed high-fat diet group (P = 0.0450). For the ApoE knockout mice, the arachidonic acid contents in the CS2-exposed normal diet group were significantly lower than those in the CS2-unexposed control diet group (P = 0.0452). For the ApoE knockout mice, the γ-linolenic acid contents in the CS2-exposed high-fat diet group were significantly higher than those in the unexposed high-fat diet group (P = 0.0447). CONCLUSION: Exposure to CS2 can induce fatty acid metabolism disorder in mice, indicating that CS2 may increase the risk of atherosclerosis and other cardiovascular diseases.

Sodium 3,5,6-trichloropyridin-2-ol poisoning: report of four cases.

Sodium 3,5,6-trichloropyridin-2-ol (STCP) is an important intermediate for synthesizing organophosphate insecticide chlorpyrifos. At present, chlorpyrifos is one of the world's largest species of pesticide products. Many studies have focused on the toxicity of chlorpyrifos, but few reports have looked at the toxicity mechanism of STCP. Even fewer studies have looked at STCP poisoning. With increasing production and usage of STCP, the chances of such poisoning will increase. In this study, we present a report on four workers who helped in the industrial manufacture of STCP and who were affected by exposure to it. We hope that these case studies will provide a foundation for further research into STCP.

[Prognosis value of urine paraquat semi-quantitative in the patients with acute paraquat poisoning].

OBJECTIVE: To investigate the relationship between semi-quantification of urine paraquat and the severity of acute paraquat poisoning, and to evaluate the prognostic value of the test in patients with acute paraquat poisoning. METHODS: A total of 179 patients with acute paraquat poisoning were categorized into four groups according to their semi-quantification results of urine paraquat: +group (n = 36), ++group (n = 23), +++ group (n = 25), and ++++group (n = 95). The clinical features, severity of hepatic and renal injuries, respiratory failure, and clinical classification were compared between these four groups. Kaplan-Meier analysis was used to evaluate the survival rate. RESULTS: The 60-day mortality was 45.25% (81/179). The amount of ingestion increased significantly from +group to ++++group (P < 0.05). No patient in +group was found to have serious complications, while most patients in ++++group suffered organ dysfunction or even organ failure. The incidence of acute respiratory failure, renal failure, and hepatic failure in ++++group was significantly higher than that in +group, ++group, and +++group (P < 0.05). The urine paraquat concentration was positively correlated with the clinical severity of acute paraquat poisoning (Spearman correlation coefficient = 0.720, P < 0.01). Kaplan-Meier survival analysis showed that the mortality of ++++group (73.7%) was significantly higher than that of +++group (40%), ++group (4.3%), and +group (0%) (P < 0.05). CONCLUSION: The semi-quantification of urine paraquat is a promising test in evaluating the severity of acute paraquat poisoning. This test can be used to guide therapy and to predict the outcomes of patients suffering acute paraquat poisoning.

[Comparison analysis on remedy condition of acute chemical intoxication in emergency departments and occupational departments of general hospitals].

OBJECTIVE: To investigate the current situation of treatment for acute chemical poisoning in the emergency departments and occupational disease departments of some general hospitals and to provide a basis for improving the ability of general hospital to deal with acute chemical poisoning. METHODS: Four hospitals from Shandong Province, Beijing City, and Shanxi Province, China were selected in the study. They included two first-class hospitals located in the downtown, where the patients with acute chemical poisoning from urban and suburban areas were admitted to the occupational disease departments, and two second-class hospitals located in the suburban area or county, where the patients with acute chemical poisoning from the suburban area were admitted to the emergency departments. A questionnaire survey was conducted in 141 medical workers (51 persons in the emergence department group and 90 persons in the occupational disease department group) that were engaged in the treatment of acute chemical poisoning in the four hospitals; 1999 medical records were analyzed. Individual in-depth interviews, questionnaire investigation, and field observation were used to compare the emergency department group and occupational disease department group in terms of the ability to deal with acute chemical poisoning and the training on treatment for acute chemical poisoning. RESULTS: The emergency department group had significantly higher proportion of pesticide poisoning cases than the occupational disease department group (P<0.01). Thirty-seven of the patients in occupational disease department group died, with a fatality rate of 2.7%, and 14 of the patients in emergence department group died,with a fatality rate of 2.2%, so there was no significant difference between the two groups in this regard (P>0.05). There were significantly more cases treated without emergency plan in the emergency department group than in the occupational disease department group ( 37.3% vs. 10.0%, P <0.0 1). The occupational disease department group had significantly higher score of knowledge about the treatment for acute chemical poisoning than the emergence department group (7.2±1.3 vs. 5.2±0.9, P<0.01 ). There were significantly lower proportions of medical staff who had received training on the knowledge about acute chemical poisoning and on the emergency disposal of acute chemical poisoning in the emergency department group than in the occupational disease department group (P<0.05). CONCLUSION: There is a lack of the knowledge about treatment for acute chemical poisoning and protective measures during treatment among the medical staff in general hospitals, and related training and emergency plan are needed.

[Determination method for 17 pesticides in common in whole blood by gas chromatography coupled to mass spectrometry with solid-phase extraction sample cleanup].

OBJECTIVE: To establish a method for simultaneous determination of 17 common pesticides in whole blood by solid phase extraction-gas chromatography-mass spectrometry (SPE-GC-MS). METHODS: Whole blood samples were treated by extraction with acetonitrile, and the obtained extract was cleaned up using an Oasis HLB SPE cartridge; pesticides were separated by GC and quantitatively analyzed by MS with selected ion monitoring. RESULTS: The concentrations of 17 pesticides in whole blood were 1.0-5.0 mg/L, and the recovery rate was 41.3-102.1%, with a relative standard deviation of less than 10%in most pesticides. The 17 pesticides showed a good linear relationship between concentration and peak area within 0.5-5.0 mg/L, with a correlation coefficient of 0.9945-0.9994. The limit of detection and limit of quantification were 0.02-0.05 mg/L and 0.05-0.09 mg/L, respectively. CONCLUSION: With this method, 17 pesticides in whole blood can be well separated and determined. This method has high sensitivity, accuracy, and precision and can be used for identification and quantification of multiple pesticides in blood samples.

[Expression of serum cytokines in patients with pneumoconiosis by antibody chip].

OBJECTIVE: To investigate the changes in expression of serum cytokines in patients with pneumoconiosis using cytokine antibody chips (CACs). METHODS: The CAC technology was applied to measure the serum levels of 60 cytokines in 12 patients with pneumoconiosis and 3 normal controls. RESULTS: In the patients with pneumoconiosis, the highly expressed serum cytokines included interleukin (IL)-1α, IL-1ß, IL-2, ILs 4-16, macrophage colony-stimulating factor, interferon-γ, tumor necrosis factor (TNF)-α, TNF-ß, human bone morphogenetic protein-6, fibroblast growth factor-7, neurotrophin-3, and stem cell factor, and the lowly expressed serum cytokines included recombinant human I-309, monocyte chemoattractant protein (MCP)-1, MCP-2, MCP-3, MCP-4, macrophage inflammatory protein (MIP)-1-δ, and MIP-3-α. CONCLUSION: Patients with pneumoconiosis have changes in the expression of most serum cytokines.

[Determination of lead and isotope ratios in whole blood by inductively coupled plasma mass spectrometry].

OBJECTIVE: To establish a method to determine lead and Isotope Ratios in whole blood by inductively coupled plasma mass spectrometry (ICP-MS). METHODS: The whole blood samples was removed protein by 5% nitric acid , Online join thallium (Tl) as internal standard substance, used lyophilized bovine blood lead and cadmium standard material (GBW09139h and GBW09140h) for quality control of blood lead concentrations. Lead isotope standard substances (GBW04426) is used to determine the correction factor, lead isotope ratios will lead isotope standard reference material NIST SRM981 by icp-ms with samples for testing. RESULTS: Optimize the detection method, detection of blood lead and lead isotope, and the method of linear range r >0.9999, GBW09139h and GBW09140h test results are within the scope of quality control. NIST SRM981 isotope determination precision RSD<1%, NIST SRM981 test results and the certificate of value close to. CONCLUSION: The method is simple and convenient data is reliable, can meet the total lead (pb) in blood and former isotope simultaneous determination.

[The rescue modalities and etiology of acute organic solvent poisoning].

OBJECTIVE: To investigate the rescue modalities and etiology of acute organic solvent poisoning. METHODS: A total of 776 cases of acute organic solvent poisoning were analyzed retrospectively. The kinds of organic solvents, the modes of exposure, the characteristics of poisoning and the methods of treatment were analyzed. RESULTS: Poisoning was due to occupational exposure to organic solvents in 87.4%, the other was exposed in daily life. The total number of organic solvents harming the patients was 55. The most common three of the organic solvent poisoning were halogenated hydrocarbons poisoning, hydrocarbons poisoning, amino- and nitro-hydrocarbons poisoning. The accidents of mass poisoning were increasing in numbers recently, especially the acute halogenated hydrocarbons poisoning. CONCLUSION: To know the numerous poisonings responsible for acute solvent poisoning is essential for enhancing the pre-hospital care, emergency treatment and following treatment. Also, extensive clinical knowledge and numerous biologic laboratory tests are needed to improve the diagnosis and rescue of acute solving poisoning. Effect of therapeutic plasma exchange treatment on sever acute poisoning is with a positive attitude.

[Measurement of 16 elements in blood by inductively coupled plasma mass spectrometry].

OBJECTIVE: To establish a method of determining more elements in whole blood by inductively coupled plasma mass spectrometry (ICP-MS). METHODS: The whole blood samples were treated by 5% nitric acid to remove the proteins, then were centrifuged. Sixteen elements (Be, Al, Mn, V, Cr, Co, Ni, As, Mo, Ag, Cd, Sb, Ba,Tl, Pb and U) in the supernatant were directly measured by ICP-MS. RESULTS: The detection limits of 16 elements were 0.01 ∼ 6.51 µg/L. The linear correlation coefficient was ≥ 0.999. The relative standard deviations were below 5 %. The recovery rates were 105% ∼ 115%. Seronorm Trace Elements SerumL-1 LOT 0903106 and GBW09139g or GBW09140g were used in the quality control, the detected results corresponded with the standard values. CONCLUSION: ICP-MS technique is a simple, rapid, accurate and reliable method, which can be used to measure several trace elements in whole blood samples.

[Application of auditory brainstem response (ABR) and 40 Hz auditory event related potential (40 Hz AERP) to the diagnosis of occupational noise-induced hearing impairment].

OBJECTIVE: To investigate the application of auditory brainstem response (ABR) and 40 Hz auditory event related potential (40 Hz AERP) to the diagnosis of occupational noise-induced hearing impairment and to provide the evidence for diagnosis of occupational deafness. METHODS: Pure tone audiometry, ABR and 40 Hz AERP were performed in 54 workers occupationally exposed to noise. The thresholds of higher frequency band, 3 kHz and 4 kHz were compared with the threshold of ABR. The thresholds of auditory frequency ban and 0.5 kHz were compared with the threshold of 40 Hz AERP. RESULTS: A better correlation was found between thresholds of ABR and higher frequency pure tone audiometry. There was a significant difference of thresholds between 40 kHz AERP and pure tone audiometry. The correction values of thresholds between 40 kHz AERP and pure tone audiometry in the light noise-induced hearing impairment group and the moderate noise-induced hearing impairment group were (16.43 ± 1.08) and (11.80 ± 1.12) dBn HL, respectively. CONCLUSION: In diagnosis of occupational noise-induced hearing impairment, the threshold of ABR can be used to estimate the hearing threshold of pure noise higher frequency. Because there is the significant difference of the thresholds between pure tone audiometry and 40 Hz AERP, the response threshold can not be served as the audiometry threshold, and the behavioral hearing thresholds can only be obtained by adjusting the response threshold with respective correction value.

[Evaluation of different oxygen therapies on therapeutic effects in rats with acute carbon dioxide poisoning].

OBJECTIVE: To study therapeutic effects by using different oxygen therapies in rats with acute carbon dioxide poisoning, to select the best oxygen therapy technology for patients with acute carbon dioxide poisoning on the spot. METHODS: Sixty healthy male Sprague-Dawley rats were randomized into normal control group, carbon dioxide exposure group, hyperbaric oxygen treatment group (pressure 2 ATA, FiO(2)100%), high concentration of atmospheric oxygen treatment group (FiO(2)50%), low concentration of atmospheric oxygen treatment group (FiO(2)33%). After treated with different oxygen in rats with acute carbon dioxide poisoning, arterial pH, PO2 and PCO2 of rats were detected, in addition observe pathological changes of lung tissue and brain tissue. RESULTS: The arterial pH (7.31 ± 0.06) and PO2 [(68.50 ± 15.02) mm Hg] of carbon dioxide exposure group were lower than those of control group [pH (7.42 ± 0.02) and PO2 (92.83 ± 8.27) mm Hg], PCO2 [(71.66 ± 12.10) mm Hg] was higher than that of control group [(48.25 ± 2.59) mm Hg] (P < 0.05); the arterial pH (hyperbaric oxygen treatment group 7.37 ± 0.02, high concentration of atmospheric oxygen treatment group 7.39 ± 0.03, low concentration of atmospheric oxygen treatment group 7.38 ± 0.02) and PO2 of oxygen treatment groups [hyperbaric oxygen treatment group, high concentration of atmospheric oxygen treatment group, low concentration of atmospheric oxygen treatment group were (82.25 ± 12.98), (84.75 ± 11.24), (83.75 ± 16.77) mm Hg, respectively] were higher than that of carbon dioxide exposure group, PCO2 [hyperbaric oxygen treatment group, high concentration of atmospheric oxygen treatment group, low concentration of atmospheric oxygen treatment group were (52.25 ± 4.95), (51.75 ± 4.82), (52.66 ± 5.61) mm Hg, respectively] was lower than that of carbon dioxide exposure group (P < 0.05); there was no significant difference of the arterial pH, PO2 and PCO2 between oxygen treatment groups and control group (P > 0.05); there was no significant difference of the arterial pH, PO2 and PCO2 among oxygen treatment groups (P > 0.05). There was large area of bleeding of lungs in rats with carbon dioxide poisoning, the bleeding of lungs in rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment was better than the rats with carbon dioxide poisoning, there was no abnormal appearance of lungs in rats with hyperbaric oxygen treatment. The light microscope observation showed that there were diffuse bleeding and exudation of lungs in rats with carbon dioxide poisoning, the bleeding and exudation of lungs in rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment were better than the rats with carbon dioxide poisoning, there were only minor bleeding and exudation of lungs in rats with hyperbaric oxygen treatment. There was no difference of brain in anatomy and microscopy among all groups, there were no significant bleeding, edema, cell degeneration and necrosis. CONCLUSIONS: Lung pathology in acute carbon dioxide poisoning rats with hyperbaric oxygen treatment is better than the rats with high concentration of atmospheric oxygen treatment and low concentration of atmospheric oxygen treatment, there is no significant difference of effect between high concentration of atmospheric oxygen treatment group and low concentration of atmospheric oxygen treatment group, however, the results of blood gas analysis and lung pathology than the exposure group improved, so qualified medical unit for hyperbaric oxygen therapy as soon as possible, hyperbaric oxygen treatment facilities in the absence of circumstances, the emergency treatment of early oxygen is also a good measure.

[Effect of oxygen therapy on the morphology of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication].

OBJECTIVE: To evaluate the effects of different oxygen therapy technique (different concentrations of normobaric oxygen and the hyperbaric oxygen) on the ultrastructure of cardiac muscle, lung and liver in rats with acute hydrogen sulfide intoxication. METHODS: One hundred healthy male Wistar rats were randomly divided into five groups: normal control group (A), poisoned group (B), oxygen therapy group (C), oxygen therapy group (D) and oxygen therapy group (E). After the exposure to 300 ppm H2S for 60 min in a static exposure tank (1 m3), the rats were treated with oxygen therapy, C, D and E groups were given 33% oxygen, 50% oxygen of atmospheric oxygen and hyperbaric oxygen therapy for 100 min, respectively. The rats in normal control group inhaled air under the same environment. After exposure and therapy, the tissues of lung, heart and liver were observed under light microscope and electron microscope. RESULTS: The results of light microscope examination showed that the broken and not well aligned cardiac myofilaments, cytoplasmic edema and pyknosis could be seen in group B. The well aligned and clear cardiac myofilaments appeared in group C, D and E. The alveolar hemorrhage, edema and inflammatory cells exudation could not be seen in group A. Alveolar epithelial cell edema, unsmooth alveolar edge and alveolar inflammatory cells exudation could be found in group B. The unsmooth alveolar septal borders and pulmonary edema could be seen occasionally in group C and D, the alveolar inflammatory cells exudation could not be seen in group E. The regular hepatic boards and the uniform hepatic cellular nuclei were found in group A. The disordered hepatic boards, widened cellular gaps and cytoplasmic edema could be seen occasionally in group B. The irregular hepatic boards and ballooning degeneration could be seen in group C and D. The regular hepatic boards and uniform cytoplasm could be found in group E. The results of electron microscope examination indicated that the mitochondrial swelling, autolyzing, fuzzy and breakage of myocardial cells were observed in group B; the clear mitochondrial structure appeared in group E. The apoptosis and organelle vacuole of alveolar epithelial cells could be observed in group B. The relatively normal nuclei of alveolar epithelial cells could be seen in group E. The lax cytoplast structure of hepatocytes, unclear nuclear membrane, lumped chromatin, slightly swelled mitochondria and phagosomes were observed in group B. However, no improved change was observed in group C, D and E. CONCLUSION: Hydrogen sulfide could induce the extensive and severe damage of myocardial mitochondria, alveolar epithelial cells and hepatocytes, the oxygen therapy in good time could reduce significantly the myocardial injury, and improve the lung injury to some extent. High-pressure oxygen therapy is better than the normobaric oxygen therapy.

[Evaluating the effects of different oxygen therapies on the rats with acute nitrogen asphyxia].

OBJECTIVE: To Evaluate the effects of different oxygen therapies on the rats with acute nitrogen asphyxia and to study the best oxygen therapic protocol for patients with acute nitrogen asphyxia on the spot. METHODS: Sixty healthy male Wistar rats were divided into 5 groups: control, exposure to nitrogen, 33% oxygen treatment, 50% oxygen treatment and hyperbaric oxygen treatment groups. The behavioral performance, arterial oxygen pressure (PO2), carbon dioxide partial pressure (PCO2) and oxygen saturation (SPO2), biochemical changes in liver and kidney function and myocardial enzymes in 5 groups were measured. RESULTS: The rats exposed to nitrogen firstly were excited then inactive symptoms, but consciousness was recovered after oxygen therapy. The PO2 and SPO2 in nitrogen exposure group were (79.67 +/- 9.12) and (94.92 +/- 2.78) mm Hg, respectively, which were significantly lower than those in control group (P<0.01). The PO2 and SPO2 of 3 oxygen treatment groups were (94.75 +/- 7.24), (94.92 +/- 8.98), (104.58 +/- 7.12)mm Hg and (97.17 +/- 0.83), (96.92 +/- 1.16), (97.42 +/- 0.67)mm Hg, respectively, which were significantly higher than those in nitrogen exposure group (P<0.05). The PO2 in hyperbaric oxygen treatment group was significantly higher than those in other 2 oxygen treatment groups (P<0.05). The SPO2 in hyperbaric oxygen treatment group was (51.42 +/- 6.60) mm Hg which was significantly higher than that [(44.58 +/- 3.42)mm Hg] in 50% oxygen treatment groups (P< 0.05). AST [(270.50 +/- 49.05 )U/L], ALT [(122.67 +/- 55.44 )U/L], BUN [(7.31 +/- 0.93 )mmol/L], Cr[(28.32 +/- 4.35) micromol/L], CK [(1808.42 +/- 582.05)U/L] and CtnI [(22.52 +/- 14.29 )ng/ml] in nitrogen exposure group were significantly higher than those in control group (P<0.05). AST [(165.25 +/- 30.87) U/L], HBDH [(350.83 +/- 103.00)U/L] and CtnI [(11.23 +/- 5.38) ng/ml] in hyperbaric oxygen treatment group were significantly lower than those in other 2 oxygen treatment groups (P<0.05). CONCLUSION: Timely and effective oxygen therapy can significantly increase arterial pressure of oxygen and oxygen saturation in the rats with acute nitrogen asphyxia, and can improve liver function and cardiac damage. The hyperbaric oxygen chamber can significantly increase the therapeutic effects on rats with acute nitrogen asphyxiation.

Identification of HMMR as a prognostic biomarker for patients with lung adenocarcinoma via integrated bioinformatics analysis.

BACKGROUND: Lung adenocarcinoma (LUAD) is the most prevalent tumor in lung carcinoma cases and threatens human life seriously worldwide. Here we attempt to identify a prognostic biomarker and potential therapeutic target for LUAD patients. METHODS: Differentially expressed genes (DEGs) shared by GSE18842, GSE75037, GSE101929 and GSE19188 profiles were determined and used for protein-protein interaction analysis, enrichment analysis and clinical correlation analysis to search for the core gene, whose expression was further validated in multiple databases and LUAD cells (A549 and PC-9) by quantitative real-time PCR (qRT-PCR) and western blot analyses. Its prognostic value was estimated using the Kaplan-Meier method, meta-analysis and Cox regression analysis based on the Cancer Genome Atlas (TCGA) dataset and co-expression analysis was conducted using the Oncomine database. Gene Set Enrichment Analysis (GSEA) was performed to illuminate the potential functions of the core gene. RESULTS: A total of 115 shared DEGs were found, of which 24 DEGs were identified as candidate hub genes with potential functions associated with cell cycle and FOXM1 transcription factor network. Among these candidates, HMMR was identified as the core gene, which was highly expressed in LUAD as verified by multiple datasets and cell samples. Besides, high HMMR expression was found to independently predict poor survival in patients with LUAD. Co-expression analysis showed that HMMR was closely related to FOXM1 and was mainly involved in cell cycle as suggested by GSEA. CONCLUSION: HMMR might be served as an independent prognostic biomarker for LUAD patients, which needs further validation in subsequent studies.

Utility of brain CT for predicting delayed encephalopathy after acute carbon monoxide poisoning.

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a serious complication that occurs several days or weeks after carbon monoxide (CO) intoxication. This study identified computed tomography (CT) findings in the prediction of DEACMP development. Adults with CO poisoning admitted to Beijing Chaoyang Hospital, Shenyang Ninth People's Hospital, Shanxi Second People's Hospital and Shandong Provincial Hospital in China from January 2013 to January 2016 were retrospectively analyzed. Baseline demographic and clinical characteristics were extracted from the medical records. Brain CT imaging was carried out within 24 h of admission, and an integrated CT score was calculated to semi-quantify lesion severity. Patients were followed-up for 6 months. Baseline characteristics and CT findings were compared among patients who developed DEACMP (DEACMP group) and those who did not (non-DEACMP group). The receiver operating characteristic (ROC) curve analysis was used to examine the utility of integrated CT score for predicting DEACMP. Among the 123 patients included in the analysis, 27 (22.0%) developed DEACMP. The DEACMP and non-DEACMP groups did not differ with regard to age, sex and carboxyhemoglobin (COHb) level at admission. However, compared with the non-DEACMP group, the patients in the DEACMP group had longer onset time of symptoms and duration of exposure to CO, higher acute physiology and chronic health evaluation-II (APACHE-II) score, lower Glasgow Coma Scale (GCS) score, and there was a higher proportion of patients with severe symptoms and brain CT abnormalities (81.5 vs. 51.0%; P<0.05). Integrated CT score in the DEACMP group was significantly higher than that in the non-DEACMP group (73.63 vs. 51.39; P<0.01). ROC curve was used to analyze the utility of integrated CT score in the prediction of DEACMP. The area under the ROC curve was 0.700 (95% confidence interval, 0.584-0.817; P<0.01). In conclusion, brain integrated CT score has the potential to identify DEACMP in patients.

[Clinical study on pneumoconiosis with pulmonary thromboembolism].

OBJECTIVE: To probe into the clinical features and the rescue of pneumoconiosis with pulmonary thromboembolism (PTE). METHODS: 26 patients with pneumoconiosis and PTE, male 16, female 10, were collected from June 2002 to June 2006 and 42 patients only with pneumoconiosis served as control. Tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), thrombomodulin (TM), plasma protein S, C (Ps, Pc), homocysteine (Hcy) were measured by the methods of ILISA, and antithrombin (AT-III) by chromo substrate method before and after the treatment of heparin. RESULTS: The average age of patients with pneumoconiosis and PTE was 66.0 +/- 11.9 years old. The number of patients with pneumoconiosis of degree 1, 2, 3 was 3, 16 and 7 respectively. After anticoagulant therapy of heparin, 23 were well improved, and 3 died of acute respiratory failure. Dyspnea, chest pain, hemoptysis, syncope were the conspicuous symptoms. The levels of D-Dimer (0.63 +/- 0.14 mg/L), TM (5.02 +/- 1.24 microg/L) were significantly higher than those of the control (P < 0.05), and significantly lower again after the treatment (P < 0.05). The level of AT-III (96.68 +/- 7.23%) was significantly lower than that of the control, and higher again after the treatment (P < 0.05). CONCLUSION: PTE is often developed in the elder patients with high degree of pneumoconiosis (> or = 2 degree). Clinical features are complicated and non-specific, with the high negative ratio of D-Dimer (7/26), high mortality and high complications of anticoagulant therapy.

Severe acute arsine poisoning treated by plasma exchange.

INTRODUCTION: Exposure to arsine gas can cause fatal hemolysis and multiorgan damage. Whole blood exchange transfusion and hemodialysis have been recommended to treat severe acute arsine poisoning, but are associated with significant complications and sub-optimal outcomes. Plasma exchange is another method of blood purification technique but there are no data on its use in acute arsine poisoning. This retrospective study evaluated the clinical and effects and arsenic clearance from the use of plasma exchange treatment of patients with acute arsine poisoning. METHODS: Data from patients with severe acute arsine poisoning, treated with plasma exchange from December 2000 to December 2005 were collected and analyzed. Measured laboratory factors, performed before and after plasma exchange treatment included routine biochemistry and hematology tests as well as arsenic concentrations in blood, urine, and discarded plasma. RESULTS: During the study period, 12 patients with severe acute arsine poisoning were treated with plasma exchange. Plasma exchange was performed one or two times on each patient, during which the replacement fluid was fresh frozen plasma (total volume ranged from 1,400 to 4,000 mL). The range of concentrations of arsenic in discarded plasma was 27.7 to 88.7 mg/L and the range of total arsenic removed by plasma exchange was 55.4 to 177.4 mg. Plasma exchange appears to rapidly terminate arsine-induced hemolysis and favorably modify damage to the kidneys and other organs. Laboratory factors that showed significant association with treatment response were creatine kinase, lactate dehydrogenase, blood urea nitrogen, total bilirubin, and heart-related enzymes. All patients recovered from the poisoning and were in good condition at a 2 to 3 months follow-up. CONCLUSIONS: Plasma exchange appears to be an effective treatment intervention for patients with severe acute arsine poisoning. It is suggested that it be used as early as possible.