ABSTRACT
Introduction Dysfunctional closed chest drainage unit (CDU) dysfunction is a common but serious clinical problem associated with tube thoracostomy and results in a significant rise in morbidity, prolonged hospital stays, and increased economic burden. This observational study examines the proximate factors of closed CDU dysfunction in addition to their relative frequency. Based on our findings, we suggest logical recommendations for preventing the factors that contribute to closed chest drainage unit dysfunction. Method The study target population consists of all those individuals who had experienced tube thoracostomy for any pathology related to the chest cavity treated in the Department of Thoracic Surgery, Nishter Medical University, Multan, Pakistan, from February 2015 to January 2017. The study population was not restricted by age or gender. Of the 727 examined cases, only those patients who had experienced tube thoracostomy and had significant failure in draining the pleural collection were included in the study. Detailed histories were collected, and thorough physical examinations were carried out for each participant. Chest x-rays and, if needed, computed tomography (CT) scans were obtained to properly examine the placement of the chest tubes and detect the causative factor of the closed CDU dysfunction. Results A total of 139 cases were included in the study. The most common cause of closed CDU dysfunction was the use of the wrong CDU connection (n = 24, 17.3%). Other common problems included inadequate prime fluid use, loose connections, kinked tubes, and overly full bottles. Conclusion Closed CDU dysfunction may be prevented by adopting and following proper protocols for tube thoracostomy.
ABSTRACT
BACKGROUND: Dabigatran etexilate, was found to be effective for stroke prevention in patients with non-valvular atrial fibrillation. Given its predictable pharmacodynamics, laboratory monitoring is not required. Moreover, the risks of overall bleeding, intracranial bleeding, and life-threatening hemorrhage from dabigatran were found to be lower than warfarin. However, a higher risk of gastrointestinal (GI) bleeding caused by dabigatran from the randomized evaluation of long-term anticoagulant therapy (RE-LY) trial has raised the concern regarding clinical outcomes of patients with GI bleeding caused by dabigatran compared with warfarin. METHODS: We retrospectively studied patients who were hospitalized for GI bleeding from dabigatran compared with warfarin with therapeutic anticoagulation monitoring during 2009 to 2012. Initial laboratory findings at presentation, number of transfused packed red blood cells (PRBCs), acute kidney injury, clinical outcomes (e.g., hypotension, tachycardia), length of stay, and death were compared. RESULTS: Thirteen patients taking dabigatran and 26 patients who were on warfarin with therapeutic international normalized ratio (INR) were hospitalized during the study period. Demographic data and baseline parameters between the two groups were not significantly different except for concurrent aspirin use (84.6% vs. 50%, P=0.036). Fifty-four percent of patients taking dabigatran did not have activated partial thromboplastin time (aPTT) level performed at presentation (7/13). The patients with GI bleeding from warfarin received significantly more PRBC transfusions compared with the dabigatran group (1.92±2.2 vs. 0.69±1.1 units, P=0.024). After controlling for initial hemoglobin and history of chronic kidney disease by using multivariate analysis, the patients in the warfarin group were likely to receive more PRBC. Hypotension at presentation was more common in GI bleeding caused by warfarin than dabigatran but the P value was insignificant (30.8% vs. 7.7%, P=0.11). Nevertheless, no differences in clinical outcomes or length of stay were found between the two groups. CONCLUSIONS: From our data, the patients with GI bleeding from dabigatran were likely to receive fewer PRBC transfusions; however, clinical outcomes and length of stay were comparable to GI bleeding caused by warfarin. Our sample generalizes to an elderly population (mean age of 77.9±10 years old) with creatinine clearance (CrCl) >30 mL/min who experience GI bleeding during chronic anticoagulation.
ABSTRACT
BACKGROUND: Motor vehicle crashes are a leading cause of mortality in the United States, although seat belts significantly reduce the risk of death. Police officers do not always wear a seat belt. A retrospective study was conducted on all crashes that involved marked police vehicles in the United States and included a death in any of the involved vehicles. METHODS: For the years 1997 through 2001, crash data were collected and analyzed from the Fatality Analysis Reporting System that included an isolated or multiple vehicle crash with a marked police vehicle and a resulting death in any of the involved vehicles. Motorcycle, aircraft, and undercover police crashes were excluded from this study. Only the occupants of the police vehicle involved in the crash were included in the study. In addition, crashes involving police vehicles where the status of seat belt use by the occupants of the police vehicle was unknown were also excluded. RESULTS: When the crashes occurred, 59.9% of the officers were responding to nonemergency calls, 79.8% of the occupants were wearing their seat belts, and 79.5% survived. Of the 104 occupants that were not belted, 42 (40.4%) died in the crash, compared with 64 (15.5%) of the 412 belted occupants (risk ratio, 2.6; odds ratio, 3.7). CONCLUSION: The risk of death was 2.6 times higher for unbelted occupants of police vehicles than for belted occupants in our study population. In addition, seat belt use was not statistically related to emergency versus nonemergency calls.