Gardner, Lindsay B.

Factor VII (FVII) is an important, vitamin K-dependent clotting factor. Acquired FVII deficiency is a rare entity that is associated with serious bleeding complications. We report a case of acquired FVII deficiency in a patient with recurrent chronic myeloid leukemia in blast crisis who developed bilateral retinal hemorrhages. The coagulopathy was corrected with the initiation of chemotherapy and subsequent reduction in peripheral blast count.

Rationale, aims, and objectives: Post-hospitalization follow-up within 30 days following discharge has been shown to positively impact time to readmission, healthcare costs, and patient self-reported adherence and satisfaction. We aimed to improve resident satisfaction with the process of establishing post-hospitalization, primary care provider (PCP) follow-up. Methods: In this quality improvement study we surveyed all internal medicine residents at our institution regarding their satisfaction with the process of establishing PCP follow-up at the time of hospital discharge. A streamlined process was developed and two subsequent interventions were enacted; a dedicated teaching session and distribution of pocket cards outlining the process. Residents were then surveyed following each intervention to assess for impact on overall satisfaction and burden of work. Results: Initially, 77.3% of residents were not satisfied with the process of establishing post-hospitalization PCP follow-up. Following the first intervention there was a trend towards increasing satisfaction rates by 16.7% (p= 0.20), and after the second intervention there was a statistically significant increase in satisfaction rates from baseline by 44% (p= 0.007). There was also a reduction in the feeling of workload burden associated with establishing PCP follow-up from 32% to 25%, and over 67% of participants either agreed or strongly agreed that the workload was not too burdensome. Conclusion: This quality improvement initiative established that resident physicians at our institution previously found the process of establishing PCP follow-up at the time of patient discharge both confusing and burdensome. Through the implementation of our interventions we were able to achieve our aims of improving resident satisfaction.

We report a case of a catheter-related bloodstream infection due to oxacillin-susceptible Staphylococcus pseudintermedius in a patient receiving haemodialysis who possibly acquired the organism from her pets. Because of persistent bacteremia and the organism’s ability to form biofilm, catheter removal and antimicrobial therapy were indicated to attain source control. Both clinical and microbiological cure were confirmed. Catheter care education should include information about pet exposure and the possibility of zoonotic infections.

Blood-brain barrier (BBB) dysfunction in acute liver failure (ALF) results in increased BBB permeability that often precludes the patients from obtaining a life-saving liver transplantation. It remains controversial whether matrix metalloproteinase-9 (MMP-9) from the injured liver contributes to the deregulation of BBB function in ALF. We selectively upregulated a physiologic inhibitor of MMP-9 (TIMP-1) with a single intracerebroventricular injection of TIMP-1 cDNA plasmids at 48 and 72 hours, or with pegylated-TIMP-1 protein. Acute liver failure was induced with tumor necrosis factor-α and D-(+)-galactosamine in mice. Permeability of BBB was assessed with sodium fluorescein (NaF) extravasation. We found a significant increase in TIMP-1 within the central nervous system (CNS) after the administration of TIMP-1 cDNA plasmids and that increased TIMP-1 within the CNS resulted in an attenuation of BBB permeability, a reduction in activation of epidermal growth factor receptor and p38 mitogen-activated protein kinase signals, and a restoration of the tight junction protein occludin in mice with experimental ALF. Pegylated TIMP-1 provided similar protection against BBB permeability in mice with ALF. Our results provided a proof of principle that MMP-9 contributes to the BBB dysfunction in ALF and suggests a potential therapeutic role of TIMP-1 in ALF.