Thromboprophylaxis in hospitalized trauma patients: a systematic review and meta-analysis of implementation strategies.

Introduction: Venous thromboembolism (VTE) prophylaxis implementation strategies are well-studied in some hospitalized medical and surgical patients. Although VTE is associated with substantial mortality and morbidity in trauma patients, implementation strategies for the prevention of VTE in trauma appear to be based on limited evidence. Therefore, we conducted a systematic review and meta-analysis of published literature on active implementation strategies for VTE prophylaxis administration in hospitalized trauma patients and the impact on VTE events. Methods: A systematic review and meta-analysis was performed in adult hospitalized trauma patients to assess if active VTE prevention implementation strategies change the proportion of patients who received VTE prophylaxis, VTE events, and adverse effects such as bleeding or heparin-induced thrombocytopenia as well as hospital length of stay and the cost of care. An academic medical librarian searched Medline, Scopus, and Web of Science until December 2022. Results: Four studies with a total of 1723 patients in the active implementation strategy group (strategies included education, reminders, human and computer alerts, audit and feedback, preprinted orders, and/or root cause analysis) and 1324 in the no active implementation strategy group (guideline creation and dissemination) were included in the analysis. A higher proportion of patients received VTE prophylaxis with an active implementation strategy (OR=2.94, 95% CI (1.68 to 5.15), p<0.01). No significant difference was found in VTE events. Quality was deemed to be low due to bias and inconsistency of studies. Conclusions: Active implementation strategies appeared to improve the proportion of major trauma patients who received VTE prophylaxis. Further implementation studies are needed in trauma to determine effective, sustainable strategies for VTE prevention and to assess secondary outcomes such as bleeding and costs. Level of evidence: Systematic review/meta-analysis, level III. PROSPERO registration number: CRD42023390538.

Spontaneous small bowel perforation: a rare GI manifestation of type IV Ehlers-Danlos syndrome.

Isolated small bowel perforation is low in the differential diagnosis of abdominal pain in the young, relatively healthy patient. It is, however, a rare manifestation of type IV (vascular) Ehlers-Danlos syndrome (EDS). In addition, there is no general consensus on the management of GI manifestations in patients with type IV EDS. We present the case of a 31-year-old male with history of type IV EDS, presenting with acute onset abdominal pain. Imaging was notable for intra-abdominal free air and thickened loops of small bowel in the pelvis. The patient underwent exploratory laparotomy with resection of the small bowel perforation with enteroenteric anastomosis. In our literature review, we evaluated gastrointestinal manifestations observed in patients with type IV EDS, management recommendations and potential complications to be mindful of in this population.

Potential widespread denitrosylation of brain proteins following prolonged restraint: proposed links between stress and central nervous system disease.

The biochemical pathways by which aberrant psychophysiological stress promotes neuronal damage and increases the risks for central nervous system diseases are not well understood. In light of previous findings that psychophysiological stress, modeled by animal restraint, can increase the activities and expression levels of nitric oxide synthase isoforms in multiple brain regions, we examined the effects of restraint, for up to 6 h, on levels of S-nitrosylated proteins and NOx (nitrite + nitrate), a marker for high-level nitric oxide generation, in the brains of rats. Results identify functionally-diverse protein targets of S-nitrosylation in the brain, in vivo, and demonstrate the potential for widespread loss of protein nitrosothiols following prolonged restraint despite a concomitant increase in NOx levels. Since physiological levels of protein S-nitrosylation can protect neurons by maintaining redox homeostasis, by limiting excitatory neurotransmission, and by inhibiting apoptotic and inflammatory pathways, we propose that over-activation of protein denitrosylation pathways following sustained or repeated stress may facilitate neural damage and early stages of stress-related central nervous system disease.