Pericardial tamponade can lead to significant hemodynamic derangement including cardiac arrest. We experienced a case of pericardial tamponade in a patient with end-stage renal disease. Hemodynamic changes occurred by unexpectedly aggravated pericardial effusion during surgery for iatrogenic hemothorax. We quickly administered a large amount of fluids and blood products for massive bleeding and fluid deficit due to hemothorax. Pericardial effusion was worsened by massive fluid resuscitation, and thereby resulted in pericardial tamponade. Hemodynamic parameters improved just after pericardiocentesis, and the patient was transferred to the intensive care unit.
Cardiac Tamponade ; Heart Arrest ; Hemodynamics ; Hemorrhage ; Hemothorax ; Humans ; Intensive Care Units ; Kidney Failure, Chronic ; Pericardial Effusion ; Pericardiocentesis ; Resuscitation

PURPOSE: We designed our study to find optimal timing for tracheostomy, and to determine the effects of early tracheostomy on clinical courses in flame burned patients with inhalation injury. METHODS: A retrospective chart review was completed for adult patients admitted to Hangang Sacred Heart Hospital Burn Center, Hallym University Medical Center, Seoul, Korea, between March 1, 2004 and February 28, 2009, who were diagnosed with flame burn with inhalation injury and who underwent tracheostomy during their hospitalization. One hundred eighteen patients were enrolled in this study. Patients were assigned to one of three groups based on the timing of tracheostomy: postburn days (PBD) 0 to 7 [Early tracheostomy (ET) group], 8 to 12 [Intermediate tracheostomy (IT) group], and greater than 13 [Late tracheostomy (LT) group]. We compared incidence of pneumonia, duration on mechanical ventilation, length of stay in intensive care unit (ICU LOS), and survival between groups. To assess the effect of tracheostomy on pulmonary function, we analyzed changes of PaO2/Fio2 (P/F) ratio. RESULTS: There were 46 patients in the ET group, 47 in the IT group and 25 in the LT group. Tracheostomy day (PBD) was 5.2+/-1.7 in ET group, 10.0+/-1.5 in IT group, and 14.8+/-1.9 in LT group (P<0.01). Statistics did not show the correlation between the timing of the tracheostomy and the incidence of pneumonia. Also mortality rate in each group showed no significant differences. There were significant differences between groups for duration on mechanical ventilation and ICU LOS (P<0.01). P/F ratio correlated with time flow showed no significant differences (P=0.10). Also there were no differences between groups in changes of P/F ratio (P=0.08). CONCLUSION: In flame burned patients with inhalation injury who require prolonged mechanical ventilation, performing tracheostomy within PBD 7 may shorten the duration on mechanical ventilation and length of stay in intensive care unit.
Academic Medical Centers ; Adult ; Burn Units ; Burns ; Heart ; Hospitalization ; Humans ; Incidence ; Inhalation ; Intensive Care Units ; Korea ; Length of Stay ; Pneumonia ; Respiration, Artificial ; Retrospective Studies ; Tracheostomy

Enterotoxigenic Bacteroides fragilis (ETBF) is a human gut commensal bacteria that causes inflammatory diarrhea and colitis. ETBF also promotes colorectal tumorigenesis in the Min mouse model. The key virulence factor is a secreted metalloprotease called B. fragilis toxin (BFT). BFT induces E-cadherin cleavage, cell rounding, activation of the beta-catenin pathway and secretion of IL-8 in colonic epithelial cells. However, the precise mechanism by which these processes occur and how these processes are interrelated is still unclear. E-cadherin form homophilic interactions which tethers adjacent cells. Loss of E-cadherin results in detachment of adjacent cells. Prior studies have suggested that BFT induces IL-8 expression by inducing E-cadherin cleavage; cells that do not express E-cadherin do not secrete IL-8 in response to BFT. In the current study, we found that HT29/C1cells treated with dilute trypsin solution induced E-cadherin degradation and IL-8 secretion, consistent with the hypothesis that E-cadherin cleavage causes IL-8 secretion. However, physical damage to the cell monolayer did not induce IL-8 secretion. We also show that EDTA-mediated disruption of E-cadherin interactions without E-cadherin degradation was sufficient to induce IL-8 secretion. Finally, we determined that HT29/C1 cells treated with LiCl (beta-catenin activator) induced IL-8 secretion in a dose-dependent and time-dependent manner. Taken together, our results suggest that BFT induced IL-8 secretion may occur by the following process: E-cadherin cleavage, disruption of cellular interactions, activation of the beta-catenin pathway and IL-8 expression. However, we further propose that E-cadherin cleavage per se may not be required for BFT induced IL-8 secretion.
Animals ; Bacteria ; Bacterial Toxins ; Bacteroides fragilis* ; Bacteroides* ; beta Catenin ; Cadherins* ; Cell Transformation, Neoplastic ; Colitis ; Colon ; Diarrhea ; Edetic Acid ; Epithelial Cells ; Fibrinogen ; Humans ; Interleukin-8* ; Metalloendopeptidases ; Mice ; Trypsin