Résumé
Objective:To study the clinical characteristics of neonatal gastric perforation (NGP) and risk factors of mortality.Methods:From January, 2015 to December, 2021, clinical manifestations of neonates diagnosed with NGP in the Department of Neonatology and Neonatal Surgical Intensive Care Unit of our hospital were retrospectively analyzed. Neonates were assigned into the survival group and the death group according to their prognosis. Risk factors of mortality were analyzed using multivariate logistic regression method.Results:A total of 50 cases were enrolled, including 41 in the survival group and 9 in the death group. 38 cases were males, 34 were premature infants, 30 were low birth weight infants and 5 had history of asphyxia. The clinical manifestations included abdominal distension, tachypnea, cyanosis, poor response, fever, diminished bowel sound and redness of the abdominal wall. Abdominal X-ray indicated pneumoperitoneum. Laboratory abnormalities included leukocytosis, thrombocytopenia, elevated C-reactive protein and procalcitonin, decreased blood pH and increased lactic acid. 30 cases had perforation at the greater curvature of stomach. Perforation was larger than 3 cm in 40 cases and intestinal necrosis was identified in 14 cases. Some patients suffered from sepsis, respiratory failure, pulmonary hemorrhage, shock, coagulopathy and other related complications. The death group had significantly higher incidences of dyspnea, fever, elevated procalcitonin, blood pH<7.3, intestinal necrosis, time from onset of clinical manifestations to operation (Tm-o) >24 h and complications than the survival group ( P<0.05). Multivariate logistic regression analysis showed that pH<7.3 ( OR=9.755, 95% CI 1.363-69.800), Tm-o>24 h (OR=11.831, 95%CI 1.305-107.301), septic shock and sepsis ( OR=29.622, 95% CI 3.728-235.369) were risk factors of mortality. Conclusions:The main manifestations of NGP are abdominal distension and pneumoperitoneum. The risk factors of mortality in NGP are sepsis, blood pH<7.3 and Tm-o>24 h.
Résumé
Objective To investigate the effect of concurrent exercise intervention in metabolic endotoxemia induced by high-fat diet in rats,and further understand the damage of liver mitochondrial ultramicrostructure.Methods Eighteen SD rats with the weight of 100g were randomly divided into 3 groups:group A (standard diet group),group B(high-fat diet group) and group C (treadmill-trained group with high-fat diet).Training (1 hour/d) initiated at the same time as the HF diet was fed.After being raised for 6 weeks,the rats was euthanized and weighed up.Blood samples were taken and the levels of serum lipid were detected.The levels of serum endotoxin were detected by enzyme-linked immunoadsorbent assay.The membrane potentials of isolated mitochondrion were detected by flow cytometry instrument and the morphologic changes in mitochondria in liver were observed by electronic microscopy.Results In group B,the levels of endotoxin increased significantly(2.916 ± 0.761 rs 5.454 ± 1.254,t =-4.236,P ＜ 0.05),and the liver mitochondrial density and membrane potential also increased significantly compared with group A after 6 weeks (4.330 ±0.501 vs 3.507 ±0.532,t =2.759,P ＜0.05;l.660 ±0.202 vs 0.473 ±0.064,t =13.712,P ＜0.05).But there was no markedly different in serum endotoxin between group B and group C (4.972 ± 1.757 vs 5.454 ± 1.254,t =-0.547,P ＞ 0.05).Compared with group B,the liver mitochondrial density of group C decreased significantly (4.330±0.501 vs 3.581 ±0.188,t =3.426,P ＜ 0.05).The mitochondrial ultrastructurctural changes in each group were not obvious.Conclusions The rats fed with high-fat diet for 6 weeks can reach the state of metabolic endotoxemia.The increasing levels of the liver mitochondrial membrane potential caused by metabolic endotoxin may affect the happening and development of other diseases in the future.Concurrent exercise can not decrease the level of endotoxin.It also shows that metabolic disease caused by high-fat diet should be prevented by moderation in eating and drinking.