Faculty Bibliography

Background: The failure of recent generations of physicians to be proficient in physical diagnosis is well known in the medical community, and recently even the mainstream(Image presented) media have taken to reporting on the problem. However, the medical literature does not offer guidance to programs interested in improving the education of physical diagnosis. Purpose: To describe the peer-led curriculum implemented at our institution to teach cardiac physical diagnosis to hospitalists and house staff. Description: Our institution has created a peer-led curriculum to enhance the teaching of the cardiac physical examination that focuses on faculty development. The curriculum consists of a series of lectures and regular bedside rounds led by experienced hospitalists and cardiologists. Lecture topics include heart sounds, murmurs, and examination of the precordium and neck veins. Lectures on physical diagnosis are evidence based and supplemented with heart sounds played through a loudspeaker so learners can hear and see cardiac findings. Bedside teaching is enhanced with an electronic stethoscope wired for simultaneous auscultation with a group of learners and an iPod application that displays real-time phonocardiography (Fig. 1). These same tools allow for bedside teaching to be transferred easily to a variety of conference-based settings such as morning report or physical diagnosis-themed lectures. Conclusions: Implementation of a cardiac physical diagnosis curriculum aimed at hospitalists is an effective way to improve the education of faculty, house staff, and medical students, offers an opportunity for scholarship, and may improve patient care

The long-term complications of acute deep venous thrombosis (DVT) include recurrence, increased mortality, and the development of the postthrombotic syndrome. Rates of recurrent venous thromboembolism (VTE) are elevated in patients with cancer and thrombophilia. Heparin, administered either as unfractionated or low-molecular weight, is indicated for at least five days for acute DVT. Long-term treatment is currently a vitamin K antagonist with a variable duration depending on the etiology of the DVT and risk of bleeding. Novel anticoagulant agents that target factor Xa and directly inhibit thrombin are being studied in clinical trials and may one day replace vitamin K antagonists for the long-term treatment of VTE.Interventional approaches such as percutaneous mechanical thrombectomy have the potential to reduce clot burden in acute DVT with lower bleeding risks and help prevent development of the postthrombotic syndrome, a common and potentially debilitating complication of DVT

The chronic constriction injury model of mononeuropathy is a direct, partial nerve injury yielding thermal hyperalgesia. The inflammation that results from this injury is believed to contribute importantly to both the neuropathological and behavioral sequelae. This study involved administering a single dose (250 ng) of interleukin-10 (IL-10), an endogenous anti-inflammatory peptide, at the site and time of a chronic constriction injury (CCI) lesion to determine if IL-10 administration could attenuate the inflammatory response of the nerve to CCI and resulting thermal hyperalgesia. In IL-10-treated animals, thermal hyperalgesia was significantly reduced following CCI (days 3, 5 and 9). Histological sections from the peripheral nerve injury site of those animals had decreased cell profiles immunoreactive for ED-1, a marker of recruited macrophages, at both times studied (2 and 5 days post-CCI). IL-10 treatment also decreased cell profiles immunoreactive for the pro-inflammatory cytokine tumor necrosis factor alpha (TNF-alpha) at day 2, but not day 5. Qualitative light microscopic assessment of neuropathology at the lesion site did not suggest substantial differences between IL-10 and vehicle-treated sections. The authors propose that initial production of TNF-alpha and perhaps other proinflammatory cytokines at the peripheral nerve lesion site importantly influences the long-term behavioral outcome of nerve injury, and that IL-10 therapy may accomplish this by downregulating the inflammatory response of the nerve to injury.