The Demands of Surgery Residency: More Than Just Duty Hours?

INTRODUCTION: Efforts to improve surgical resident well-being could be accelerated with an improved understanding of resident job demands and resources. In this study, we sought to obtain a clearer picture of surgery resident job demands by assessing how residents distribute their time both inside and outside of the hospital. Furthermore, we aimed to elucidate residents' perceptions about current duty hour regulations. METHODS: A cross-sectional survey was sent to 1098 surgical residents at 27 US programs. Responses regarding work hours, demographics, well-being (utilizing the physician well-being index), and perceptions of duty hours in relation to education and rest, were collected. Data were evaluated using descriptive statistics and content analysis. RESULTS: A total of 163 residents (14.8% response rate) were included in the study. Residents reported a median total patient care hours per week of 78.0 h. Trainees spent 12.5 h on other professional activities. Greater than 40% of residents were "at risk" for depression and suicide based on physician well-being index scores. Four major themes associated with education and rest were identified: 1) duty hour definitions and reporting mechanisms do not completely reflect the amount of work residents perform, 2) quality patient care and educational opportunities do not fit neatly within the duty hour framework, 3) resident perceptions of duty hours are impacted the educational environment, and 4) long work hours and lack of adequate rest negatively affect well-being. CONCLUSIONS: The breadth and depth of trainee job demands are not accurately captured by current duty hour reporting mechanisms, and residents do not believe that their current work hours allow for adequate rest or even completion of other clinical or academic tasks outside of the hospital. Many residents are unwell. Duty hour policies and resident well-being may be improved with a more holistic accounting of resident job demands and greater attention to the resources that residents have to offset those demands.

Valproic Acid Protects Against Acute Kidney Injury in Hemorrhage and Trauma.

INTRODUCTION: Trauma is the leading cause of death among young people. These patients have a high incidence of kidney injury, which independently increases the risk of mortality. As valproic acid (VPA) treatment has been shown to improve survival in animal models of lethal trauma, we hypothesized that it would also attenuate the degree of acute kidney injury. METHODS: We analyzed data from two separate experiments where swine were subjected to lethal insults.  Model 1: hemorrhage (50% blood volume hemorrhage followed by 72-h damage control resuscitation). Model 2: polytrauma (traumatic brain injury, 40% blood volume hemorrhage, femur fracture, rectus crush and grade V liver laceration). Animals were resuscitated with normal saline (NS) +/- VPA 150 mg/kg after a 1-h shock phase in both models (n = 5-6/group). Serum samples were analyzed for creatinine (Cr) using colorimetry on a Liasys 330 chemistry analyzer. Proteomic analysis was performed on kidney tissue sampled at the time of necropsy. RESULTS: VPA treatment significantly (P < 0.05) improved survival in both models. (Model 1: 80% vs 20%; Model 2: 83% vs. 17%). Model 1 (Hemorrhage alone): Cr increased from a baseline of 1.2 to 3.0 in NS control animals (P < 0.0001) 8 h after hemorrhage, whereas it rose only to 2.1 in VPA treated animals (P = 0.004). Model 2 (Polytrauma): Cr levels increased from baseline of 1.3 to 2.5 mg/dL (P = 0.01) in NS control animals 4 h after injury but rose to only 1.8 in VPA treated animals (P = 0.02). Proteomic analysis of kidney tissue identified metabolic pathways were most affected by VPA treatment. CONCLUSIONS: A single dose of VPA (150 mg/kg) offers significant protection against acute kidney injury in swine models of polytrauma and hemorrhagic shock.

Valproic acid treatment rescues injured tissues after traumatic brain injury.

BACKGROUND: No agents that are specifically neuroprotective are currently approved to emergently treat patients with traumatic brain injury (TBI). The histone deacetylase inhibitor, high-dose valproic acid (VPA) has been shown to have cytoprotective potential in models of combined TBI and hemorrhagic shock, but it has not been tested in an isolated TBI model. We hypothesized that VPA, administered after isolated TBI, will penetrate the injured brain, attenuate the lesion size, and activate prosurvival pathways. METHODS: Yorkshire swine were subjected to severe TBI by cortical impact. One hour later, animals were randomized to VPA treatment (150 mg/kg delivered intravenously for 1 hour; n = 4) or control (saline vehicle; n = 4) groups. Seven hours after injury, animals were sacrificed, and brain lesion size was measured. Mass spectrometry imaging was used to visualize and quantitate brain tissue distribution of VPA. Sequential serum samples were assayed for key biomarkers and subjected to proteomic and pathway analysis. RESULTS: Brain lesion size was 50% smaller (p = 0.01) in the VPA-treated animals (3,837 ± 948 mm) compared with the controls (1,900 ± 614 mm). Endothelial regions had eightfold higher VPA concentrations than perivascular regions by mass spectrometry imaging, and it readily penetrated the injured brain tissues. Serum glial fibrillary acid protein was significantly lower in the VPA-treated compared with the control animals (p < 0.05). More than 500 proteins were differentially expressed in the brain, and pathway analysis revealed that VPA affected critical modulators of TBI response including calcium signaling pathways, mitochondria metabolism, and biosynthetic machinery. CONCLUSION: Valproic acid penetrates injured brain tissues and exerts neuroprotective and prosurvival effects that resulted in a significant reduction in brain lesion size after isolated TBI. Levels of serum biomarkers reflect these changes, which could be useful for monitoring the response of TBI patients during clinical studies.