ObjectiveTo investigate the clinical characteristics and contribution factors in severe coronavirus disease 2019 (COVID-19).MethodsThe clinical symptoms, laboratory findings, radiologic data, treatment strategies, and outcomes of 110 COVID-19 patients were retrospectively analyzed in these hospitals from Jan 20, 2020 to Feb 28, 2020. All patients were confirmed by fluorescence reverse transcription polymerase chain reaction. They were classified into a non-severe group and a severe group based on their symptoms, laboratory and radiologic findings. All patients were given antivirus, oxygen therapy, and support treatments. The severe patients received high-flow oxygen therapy, non-invasive mechanical ventilation, invasive mechanical ventilation or extracorporeal membrane oxygenation. The outcomes of patients were followed up until March 15, 2020. Contribution factors of severe patients were summarized from these clinical data.ResultsThe median age was 50 years old, including 66 males (60.0%) and 44 females (40.0%). Among them, 45 cases (40.9%) had underlying diseases, and 108 cases (98.2%) had different degrees of fever. The common clinical manifestations were cough (80.0%, 88/110), expectoration (33.6%, 37/110), fatigue (50.0%, 55/110), and chest tightness (41.8%, 46/110). Based on classification criteria, 78 (70.9%) non-severe patients and 32 (29.1%) severe patients were identified. Significant difference of the following parameters was found between two groups (P<0.05): age was 47 (45, 50) years vs. 55 (50, 59) years (Z=–2.493); proportion of patients with underlying diseases was 27 (34.6%) vs. 18 (56.3%) (χ2=4.393); lymphocyte count was 1.2 (0.9, 1.5)×109/L vs. 0.6 (0.4, 0.7)×109/L (Z=–7.26); C reactive protein (CRP) was 16.2 (6.5, 24.0) mg/L vs. 45.3 (21.8, 69.4) mg/L (Z=–4.894); prothrombin time (PT) was 15 (12, 19) seconds vs. 18 (17, 19) seconds (Z=–2.532); D-dimer was 0.67 (0.51, 0.82) mg/L vs. 0.98 (0.80, 1.57) mg/L (Z=–5.06); erythrocyte sedimentation rate (ESR) was 38.0 (20.8, 59.3) mm/1 h vs. 75.5 (39.8, 96.8) mm/1 h (Z=–3.851); lactate dehydrogenase (LDH) was 218.0 (175.0, 252.3) U/L vs. 325.0 (276.5, 413.5) U/L (Z=–5.539); neutrophil count was 3.1 (2.1, 4.5)×109/L vs. 5.5 (3.7, 9.1)×109/L (Z=–4.077). Multivariable logistic analysis showed that there was positive correlation in elevated LDH, CRP, PT, and neutrophil count with the severity of the disease. Currently, 107 patients were discharged and 3 patients died. Total mortality was 2.7%.ConclusionsOld age, underlying diseases, low lymphocyte count, elevated CPR, high D-dimer and ESR are relevant to the severity of COVID-19. LDH, CPR, PT and neutrophil count are independent risk factors for the prognosis of COVID-19.
Since the beginning of the coronavirus disease 2019 (COVID-19) pandemic at the end of December 2019, more than 85% of the population in China has been infected. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) mainly affects the respiratory system, especially the lungs. The mortality rate of patients with severe infection is high. A percentage of 6% to 10% of patients will eventually develop into COVID-related acute respiratory distress syndrome (CARDS), which requires mechanical ventilation and extracorporeal membrane oxygenation (ECMO) support. Some patients who survive acute lung injury will subsequently develop post COVID-19 pulmonary fibrosis (PCPF). Both fully treated CARDS and severe PCPF are suitable candidates for lung transplantation. Due to the special course, evaluation strategies are different from those used in patients with common end-stage lung disease. After lung transplantation in COVID-19 patients, special treatment is required, including standardized nucleic acid testing for the novel coronavirus, adjustment strategy of immunosuppressive drugs, and rational use of antiviral drugs, which is a big challenge for the postoperative management of lung transplantation. This consensus was evidence-based written and was reached by experts after multiple rounds of discussions, providing reference for assessment and postoperative management of patients with interstitial pneumonia after COVID-19 infection.
ObjectiveTo establish paraquat (PQ)-induced acute respiratory distress syndrome (ARDS) mice model via gavage, in order to simulate oral adminitration in clinical situations.MethodsSeventy-eight 6-8-week-old, specific pathogen free female C57 mice were chosen in this study. The mice were randomly divided into the control group (n=6) and the PQ model group(n=36); the mice in the latter group were randomly divided into 6 poisoning model subgroups further, with 6 mice in each, to find out the suitable concentration of PQ to establish stable ARDS model. The mice in the control group were given phosphatebuffer saline (PBS) by gavage, 200 μL per mouse; while the mice in the 6 poisoning model subgroups were given PQ with varies doses of 3, 10, 30, 100, 150, 300 mg/kg respectively by gavage. The clinical manifestations were observed for 7 days, and the ratio of lung wet/dry (W/D) was measured. After the suitable concentration of PQ for stable ARDS mice model was found, the other 36 mice were randomly divided into the controlgroup and the poisoning model group, both were divided into 4 subgroups, according to different observation point in time (1 day and 2, 3, 4 days after PQ gavage). The mice in the 4 control subgroups (n=3) were given PBS by gavage, 200 μL per mouse; while the mice in the 4 poisoning model subgroups (n=6) were given PQ with the suitable concentration for ARDS mice model by gavage. Pathological manifestations by Haematoxylin-Eosin staining and lung injury score were observed and analyzed.ResultsThe mice began to die at the PQ dosage of 150 mg/kg; while the death rate was stable at 300 mg/kg. On the 2nd and 4th day after PQ gavage, lung W/D was 5.335, 6.113, and 5.525, and 6.403, respectively in the mice in 150 and 300 mg/kg subgroup, which differed much from those in the control group (P<0.001). Congestion, edema, hemorrhage, alveolar structure damage, inflammation cells infiltration of lung tissue were observed, and lung injury score increased.ConclusionPQ-induced ARDS mice model by gavage is established successfully.
Objective To investigate the value of continuous blood purification （CBP）in early treatment of patients with ARDSexp （ARDS caused by extrapulmonary causes），especially in reducing inflammation mediators and extravascular lung water （EVLW）.Methods According the hospital admission sequence，the patients with APACHEⅡ scores from 15 to 20 and PaO2/FiO2 from 100 to 200 were recruited.The ARDSexp patients were divide into an intervention group treated with CBP （Mode：CVVHDF，rate of displacement liquid and dialysate：1.5 L/h，rate of blood：100-200 mL/h，and the time of CBP：72 hours），and a control group without CBP treatment. The NICO and PICCO monitoring data and the survival rates were recorded and analyzed using the SPSS software. Results The mortality rate of the intervention group was lower than that of the control group （6.3% vs. 36.8%，P=0.032）. In the 72 h monitoring dada of NICO and PICCO，the time of improving PCBF，Pm，Cdyn，VCO2，MValv，Pm，PIP，Raw，RSBI，Vd/Vt，and PaO2/FiO2 of the intervention group was severer than those in the control group，and the severety was also more than that of control group which was was significantly different at 72 h（Plt;0.05）. In the PICCO data，the time of decreasing EVWL and PVPI was shorter than the control group，and the decreasing extent was more than the control group，with significant difference at 72 h. But the changes of Apm，CI，and CVP were not significant （Pgt;0.05）. Conclusions In treatment of ARDSexp patients，CBP therapy can induce the PCBC and EVLW，improve pulmonary compliance and MValv，and reduce the mortality rate，while doesn’t influence heart function and the stability of circulation.
ObjectiveTo evaluate the effects and safety of statins in patients with acute respiratory distress syndrome (ARDS). MethodsLiteratures in English and Chinese concerning randomized controlled trials (RCTs) on statins in ARDS patients were retrieved by electronic and manual search. All related data were extracted. Meta-analysis was conducted using the statistical software RevMan 5.3 on the basis of strict quality evaluation. ResultsFive RCTs involving 1489 ARDS patients were included, with 709 patients in the statins group and 780 patients in the placebo control group. Compared with the control group, statins did not improve the survival of ARDS patients[risk ratio (RR) 1.01, 95% confidence interval (CI) 0.86 to 1.18, P=0.91), while the improvement of oxygenation[mean difference (MD) 3.92, 95%CI-14.10 to 21.94, P=0.67], ventilator-free days (MD 0.65, 95%CI-0.20 to 1.50, P=0.13) and non-pulmonary organ failure-free days (MD 1.20, 95%CI-1.46 to 3.87, P=0.38) exhibited no differences between the statins group and the control group. However statins were associated with significant elevation of creatine kinase (MD 6.92, 95%CI 5.77 to 8.07, P < 0.000 01). ConclusionThis study demonstrates that statins can not improve outcomes of ARDS patients, and the safety of statins still needs further evaluation.
Acute respiratory distress syndrome is one of the forms of respiratory failure that seriously threaten human life. It has the characteristics of very high morbidity, mortality and hospitalization costs. How to treat acute respiratory distress syndrome to improve the quality of life of patients is particularly important. Mechanical ventilation is an important treatment for acute respiratory distress syndrome. This article will review the progress in mechanical ventilation therapy for acute respiratory distress syndrome, including non-invasive mechanical ventilation and invasive mechanical ventilation (tidal volume, lung recruitment, positive end-expiratory pressure, prone position ventilation, and high-frequency oscillatory ventilation), aiming to provide basis and reference for future exploration of the treatment direction of acute respiratory distress syndrome.
Objective To observe whether additional penehycl idine hydrochloride (PHC) in mechanical ventilation produces therapeutic effect on oleic acid (OA) induced acute lung injury (ALI) in canine. Methods Seventeen male canines (weighing 12-17 kg) were divided into control group (n=5), OA group (n=6) and PHC group (n=6). ALI model was developed by central venous injection of OA in canines of OA and PHC groups. ALI model was kept steady in air, all groups received mechanical ventilation 90 minutes later. Three groups received normal sal ine 0.25 mg/kg without injection of OA(control group), normal sal ine 0.25 mg/kg after injection of OA (OA group) and PHC 0.25 mg/kg after injection of OA (PHCgroup) respectively at 0 h (90 minutes after onset time of ALI/ARDS). The heart rate (HR), mean arteial pressure (MAP), mean pulmonary arterial pressure (MPAP), central venous pressure (CVP), pulmonary artery wedge pressure (PAWP), artery blood gas analysis, cardiac output (CO), extravascular lung water index (EVLWI), FiO2 and VT were observed respectively at basel ine, onset time of ALI/ARDS and 0 h, then again at 1 hour intervals for 6 hours. Besides the above, airway peak pressure (Ppeak), airway plat pressure (Pplat), mean airway pressure (Pmean) and positve end-expriatory pressure (Peep) were also observed each hour during 1-6 hours. Oxygenation index (OI), pulmonary vascular resistance (PVR), systemic vascular resistance (SVR), alveolar-arterial differences for O2 (AaDO2) and dynamic lung compl iance (DLC) were calculated and pulmonary tissue was collected for histopathologic investigation and dry wet weight ratio (WDR) test. Results The functional parameters of PHC group were improved when compared those of OA group, but there was no siginficant difference; WDR of independent region of three groups were 80.42% ± 3.48%, 82.67% ± 4.01% and 82.26% ± 1.43% respectively; WDR of dependent region of three groups were 80.51% ± 3.60%, 83.71% ± 1.98% and 82.57% ± 1.08% respectively. WDR of PHC group were obviously improved when compared with those of OA group, but there was no significant difference. Independent and dependent regions of PHC group were significantly improved when compared those of OA group in histopathologic scores, alveolar edema, inflammatory infiltration and over-distension (P lt; 0.01). Conclusion Additional PHC in mechanical ventilation produces obvious therapeutic effect on OA induced acute lung injury in canine.