2012PubMedRequires access

[A study of the clinical features and the effect of therapy on acute respiratory distress syndrome patients as a result of severe triphosgene poisoning].

Linlin Zhang, Shusheng Zhou, Bao Liu, Zi-min Sun, Tianjun Yang, Zhu Shou-jun, Hua Fan

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Abstract

OBJECTIVE: To investigate the clinical features and treatment strategy for acute respiratory distress syndrome (ARDS) caused by phosgene. METHODS: Individualized therapy was carried out in 17 cases of severe phosgene poison patients. Blood routine, electrolytes, blood gas analysis, hepatic and renal function tests and cardiac enzymes were examined before and after treatment. RESULTS: Vital signs, fluid, electrolytes and acid-base disturbances were improved after treatment. As compared to that of pre-treatment period, white blood cells [WBC, ×10(9)/L: 12.18 ± 4.76 vs. 21.93 ± 6.21], neutrophil percentage (0.87 ± 0.05 vs. 0.92 ± 0.03), hemoglobin (Hb, g/L: 128.12 ± 25.65 vs. 173.71 ± 23.53), blood platelet count [PLT,×10(9)/L:165.12 ± 31.70 vs. 254.47 ± 70.80], alanine transaminase (ALT, U/L: 70.71 ± 46.70 vs. 212.71 ± 141.34), aspartate aminotransferase (AST, U/L: 52.47 ± 34.68 vs. 82.41 ± 34.60), blood urea nitrogen (BUN, mmol/L: 5.83 ± 4.09 vs. 7.89 ± 5.96), serum creatinine (SCr, μmol/L: 48.13 ± 14.97 vs. 67.25 ± 24.29), lactate dehydrogenase (LDH, U/L: 280.10 ± 81.77 vs. 586.35 ± 186.71), creatine kinase (CK, U/L: 199.12 ± 106.75 vs. 683.00 ± 323.21), MB isoenzyme of creatine kinase (CK-MB, U/L: 26.94 ± 9.13 vs. 45.59 ± 11.21), serum chlorine anion [Cl(-), mmol/L: 95.88 ± 6.06 vs. 102.29 ± 7.28], respiratory rate (RR, beats/min: 20.88 ± 4.30 vs. 30.06 ± 5.78), heart rate (HR, beats/min: 82.76 ± 17.16 vs. 113.35 ± 16.90), blood pH value (7.34 ± 0.44 vs. 7.39 ± 0.03) were all decreased (P < 0.05 or P < 0.01). Serum sodium ion [Na(+),mmol/L:140.61 ± 6.69 vs. 134.06 ± 4.80], arterial partial pressure of oxygen [PO(2), mm Hg, 1 mm Hg = 0.133 kPa: 84.41 ± 30.58 vs. 59.88 ± 15.19] and pulse oxygen saturation [SpO(2): 0.91 ± 0.08 vs. 0.78 ± 0.15] were increased (P < 0.05 or P < 0.01). Sixteen patients totally recovered, 1 patient died, and the cure rate was 94.12%. CONCLUSIONS: Respiratory system could be mainly injured as the result of exposure to phosgene and leading to ARDS. Early initial combination therapies with corticosteroids and respiratory support should be addressed.

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What this paper is about

OBJECTIVE: To investigate the clinical features and treatment strategy for acute respiratory distress syndrome (ARDS) caused by phosgene. METHODS: Individualized therapy was carried out in 17 cases of severe phosgene poison patients. Blood routine, electrolytes, blood gas analysis, hepatic and renal function tests and cardiac enzymes were examined before and after treatment. RESULTS: Vital signs, fluid, electrolytes and acid-base disturbances were improved after treatment. As compared to that of pre-treatment period, white blood cells [WBC, ×10(9)/L: 12.18 ± 4.76 vs. 21.93 ± 6.21], neutrophil percentage (0.87 ± 0.05 vs. 0.92 ± 0.03), hemoglobin (Hb, g/L: 128.12 ± 25.65 vs. 173.71 ± 23.53), blood platelet count [PLT,×10(9)/L:165.12 ± 31.70 vs. 254.47 ± 70.80], alanine transaminase (ALT, U/L: 70.71 ± 46.70 vs. 212.71 ± 141.34), aspartate aminotransferase (AST, U/L: 52.47 ± 34.68 vs. 82.41 ± 34.60), blood urea nitrogen (BUN, mmol/L: 5.83 ± 4.09 vs. 7.89 ± 5.96), serum creatinine (SCr, μmol/L: 48.13 ± 14.97 vs. 67.25 ± 24.29), lactate dehydrogenase (LDH, U/L: 280.10 ± 81.77 vs. 586.35 ± 186.71), creatine kinase (CK, U/L: 199.12 ± 106.75 vs. 683.00 ± 323.21), MB isoenzyme of creatine kinase (CK-MB, U/L: 26.94 ± 9.13 vs. 45.59 ± 11.21), serum chlorine anion [Cl(-), mmol/L: 95.88 ± 6.06 vs. 102.29 ± 7.28], respiratory rate (RR, beats/min: 20.88 ± 4.30 vs. 30.06 ± 5.78), heart rate (HR, beats/min: 82.76 ± 17.16 vs. 113.35 ± 16.90), blood pH value (7.34 ± 0.44 vs. 7.39 ± 0.03) were all decreased (P < 0.05 or P < 0.01). Serum sodium ion [Na(+),mmol/L:140.61 ± 6.69 vs. 134.06 ± 4.80], arterial partial pressure of oxygen [PO(2), mm Hg, 1 mm Hg = 0.133 kPa: 84.41 ± 30.58 vs. 59.88 ± 15.19] and pulse oxygen saturation [SpO(2): 0.91 ± 0.08 vs. 0.78 ± 0.15] were increased (P < 0.05 or P < 0.01). Sixteen patients totally recovered, 1 patient died, and the cure rate was 94.12%. CONCLUSIONS: Respiratory system could be mainly injured as the result of exposure to phosgene and leading to ARDS. Early initial combination therapies with corticosteroids and respiratory support should be addressed.

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Available abstract

OBJECTIVE: To investigate the clinical features and treatment strategy for acute respiratory distress syndrome (ARDS) caused by phosgene. METHODS: Individualized therapy was carried out in 17 cases of severe phosgene poison patients. Blood routine, electrolytes, blood gas analysis, hepatic and renal function tests and cardiac enzymes were examined before and after treatment. RESULTS: Vital signs, fluid, electrolytes and acid-base disturbances were improved after treatment. As compared to that of pre-treatment period, white blood cells [WBC, ×10(9)/L: 12.18 ± 4.76 vs. 21.93 ± 6.21], neutrophil percentage (0.87 ± 0.05 vs. 0.92 ± 0.03), hemoglobin (Hb, g/L: 128.12 ± 25.65 vs. 173.71 ± 23.53), blood platelet count [PLT,×10(9)/L:165.12 ± 31.70 vs. 254.47 ± 70.80], alanine transaminase (ALT, U/L: 70.71 ± 46.70 vs. 212.71 ± 141.34), aspartate aminotransferase (AST, U/L: 52.47 ± 34.68 vs. 82.41 ± 34.60), blood urea nitrogen (BUN, mmol/L: 5.83 ± 4.09 vs. 7.89 ± 5.96), serum creatinine (SCr, μmol/L: 48.13 ± 14.97 vs. 67.25 ± 24.29), lactate dehydrogenase (LDH, U/L: 280.10 ± 81.77 vs. 586.35 ± 186.71), creatine kinase (CK, U/L: 199.12 ± 106.75 vs. 683.00 ± 323.21), MB isoenzyme of creatine kinase (CK-MB, U/L: 26.94 ± 9.13 vs. 45.59 ± 11.21), serum chlorine anion [Cl(-), mmol/L: 95.88 ± 6.06 vs. 102.29 ± 7.28], respiratory rate (RR, beats/min: 20.88 ± 4.30 vs. 30.06 ± 5.78), heart rate (HR, beats/min: 82.76 ± 17.16 vs. 113.35 ± 16.90), blood pH value (7.34 ± 0.44 vs. 7.39 ± 0.03) were all decreased (P < 0.05 or P < 0.01). Serum sodium ion [Na(+),mmol/L:140.61 ± 6.69 vs. 134.06 ± 4.80], arterial partial pressure of oxygen [PO(2), mm Hg, 1 mm Hg = 0.133 kPa: 84.41 ± 30.58 vs. 59.88 ± 15.19] and pulse oxygen saturation [SpO(2): 0.91 ± 0.08 vs. 0.78 ± 0.15] were increased (P < 0.05 or P < 0.01). Sixteen patients totally recovered, 1 patient died, and the cure rate was 94.12%. CONCLUSIONS: Respiratory system could be mainly injured as the result of exposure to phosgene and leading to ARDS. Early initial combination therapies with corticosteroids and respiratory support should be addressed.

Key concepts: Medicine, ARDS, Blood urea nitrogen, Creatinine, Internal medicine, Creatine kinase, Gastroenterology, Lactate dehydrogenase

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[A study of the clinical features and the effect of therapy on acute respiratory distress syndrome patients as a result of severe triphosgene poisoning]. — Research Paper | ScholarLens