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Objective: To understand mortality and secondary outcomes in patients with both end-stage kidney disease (ESKD) and chronic limb-threatening ischemia (CLTI) after no procedural treatment, primary amputation, endovascular treatment, and open surgery., Summary Background Data: ESKD and CLTI commonly cooccur and limited prior work has demonstrated poor outcomes including one-year survival despite treatment., Methods: We conducted a retrospective national cohort study of United States Renal Data System data from January 1, 2016 to December 31, 2019 to determine mortality, major postoperative complications, and other outcomes. We performed an exploratory analysis comparing two-year survival by treatment using propensity matching., Results: Of 1,876,652 records with a CLTI diagnosis, we identified 3,908 patients with ESKD and an incident CLTI diagnosis. Mean age at CLTI diagnosis was 65.7 years and 2,405 (61.5%) were male. 2,696 (69.0%) had no procedural treatment, 609 (15.6%) had major limb amputation, 439 (11.2%) had endovascular treatment, and 164 (4.2%) had open surgery. There was 44.9% mortality at one year, along with 41.8% major postoperative complications and 52.6% readmissions at 90 days. Comparing two-year survival, we found no differences between the amputation and endovascular cohorts ( P =0.08) and between endovascular and open ( P =.06). There was superior two-year survival in the open surgery cohort compared to the amputation cohort ( P =0.002)., Conclusions: Patients living with both ESKD and CLTI experience poor outcomes irrespective of treatment. Exploratory analyses demonstrated that two-year survival among the three principal procedural treatments was similar except for superior survival among patients undergoing open therapy compared to primary amputation., Competing Interests: Conflicts of Interest: None., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Objective: Report the 2-year outcomes of a multicenter randomized controlled trial comparing robotic versus laparoscopic intraperitoneal onlay mesh ventral hernia repair., Background: Ventral hernia repair is one of the most common operations performed by general surgeons. To our knowledge, no studies have been published to date comparing long-term outcomes of laparoscopic versus robotic ventral hernia repair., Methods: The trial was registered at clinicaltrials.gov (NCT03490266). Clinical outcomes included surgical site infection, surgical site occurrence, hernia occurrence, readmission, reoperation, and mortality., Results: A total of 175 consecutive patients were approached that were deemed eligible for elective minimally invasive ventral hernia repair. In all, 124 were randomized and 101 completed follow-up at 2 years. Two-year follow-up was completed in 54 patients (83%) in the robotic arm and 47 patients (80%) in the laparoscopic arm. No differences were seen in surgical site infection or surgical site occurrence. Hernia recurrence occurred in 2 patients (4%) receiving robotic repair versus in 6 patients (13%) receiving laparoscopic repair (relative risk: 0.3, 95% CI: 0.06-1.39; P =0.12). No patients (0%) required reoperation in the robotic arm whereas 5 patients (11%) underwent reoperation in the laparoscopic arm ( P =0.019, relative risk not calculatable due to null outcome)., Conclusions: Robotic ventral hernia repair demonstrated at least similar if not improved outcomes at 2 years compared with laparoscopy. There is potential benefit with robotic repair; however, additional multi-center trials and longer follow-up are needed to validate the hypothesis-generating findings of this study., Competing Interests: S.S. receives a research grant and consulting fees paid to the institution from Activ Surgical. The original study was supported by a research grant from Intuitive. The remaining authors report no conflicts of interest., (Copyright © 2023 Wolters Kluwer Health, Inc. All rights reserved.)

Objective: The aim of this study was to compare clinical and patient-reported outcomes of robotic versus laparoscopic ventral hernia repair (LVHR) at 1-year postoperative., Summary of Background Data: Despite a relative lack of research at low risk for bias assessing robotic ventral hernia repair (RVHR), the growth of RVHR has been rapid. We previously reported short-term results of the first randomized control trial comparing RVHR versus LVHR; there was no clear difference in clinical outcomes but increased operative time and cost with robotic repair., Methods: Patients from a multicenter, blinded randomized control trial comparing RVHR versus LVHR were followed at 1 year. Outcomes included wound complication (surgical site infection, surgical site occurrence, wound dehiscence), hernia occurrence including recurrence and port site hernia, readmission, reoperation, and patient-reported outcomes (functional status, pain, and satisfaction with repair and cosmesis)., Results: A total of 124 patients were randomized and 113 patients (91%; 60 robot, 53 laparoscopic) completed 1-year follow-up. Baseline demographics were similar in both groups. No differences were seen in wound complication (15% vs 15%; P = 0.899), hernia recurrence (7% vs 9%; P = 0.576), or readmission (2% vs 6%; P = 0.251). No patients underwent reoperation in the robotic arm, whereas 5 (9%) did in the laparoscopic arm (P = 0.020). No differences were seen in patient-reported outcomes. Both arms reported clinically significant improvements in functional status, low pain scores, and high satisfaction scores at 1-year post repair., Conclusion: This study confirms that robotic ventral hernia repair is safe when compared to laparoscopy. Further studies are needed to confirm these findings., Competing Interests: SKS reports grants/payments from C-SATS and Activ Surgical. The remaining authors report no conflicts of interest., (Copyright © 2021 Wolters Kluwer Health, Inc. All rights reserved.)

Background: Ventral hernias are a common pathology encountered by surgeons. Multiple risk stratification tools have been developed in attempts to predict a patient's postoperative risk for complication. The aim of this systematic review was to identify published stratification tools, to assess their generalizability, and develop an ensemble risk score model., Methods: A systematic review of the literature was performed using PubMed and following the PRISMA guidelines. Two independent reviewers identified articles describing hernia stratification tools or validating an established tool. Inclusion criteria included articles that studied ventral hernia risk score models developed through expert consensus or from data of at least 500 subjects, performed a multivariable analysis of at least 500 patients, or assessed a previously reported model. Studies were grouped by primary outcome, and the odds ratios for correlated variables were compiled. Outcomes described in 4 or more articles were then stacked to generate a cumulative risk score model for patients undergoing abdominal wall repair., Results: A total of 20 articles were found to meet our inclusion criteria and used to develop our ensemble model. Surgical-site infection, surgical-site occurrence, and hernia recurrence were the 3 primary outcomes used to calculate our stacked cumulative risk stratification score., Conclusions: There are multiple risk score tools published; however, all have their strengths and limitations. For this reason, we created a composite score model with data from major articles to predict a patient's risk for postoperative complications. This model aims to ease the shared-decision making process for patients, surgeons, and institutions.

Researchers have attempted to link incidences of papillary thyroid cancer with radioiodine releases from nuclear power plants. Thyroid cancer detection rates are examined together with overall population exposure to ionizing radiation and actual radioiodine releases from the Indian Point Energy Center to determine if a causal relationship exists. A critical review of the statistical analyses used in previous papers is then presented.

Objectives: The devastating effect of traumatic brain injury is exacerbated by an acute secondary neuroinflammatory response, clinically manifest as elevated intracranial pressure due to cerebral edema. The treatment effect of cell-based therapies in the acute post-traumatic brain injury period has not been clinically studied although preclinical data demonstrate that bone marrow-derived mononuclear cell infusion down-regulates the inflammatory response. Our study evaluates whether pediatric traumatic brain injury patients receiving IV autologous bone marrow-derived mononuclear cells within 48 hours of injury experienced a reduction in therapeutic intensity directed toward managing elevated intracranial pressure relative to matched controls., Design: The study was a retrospective cohort design comparing pediatric patients in a phase I clinical trial treated with IV autologous bone marrow-derived mononuclear cells (n = 10) to a control group of age- and severity-matched children (n = 19)., Setting: The study setting was at Children's Memorial Hermann Hospital, an American College of Surgeons Level 1 Pediatric Trauma Center and teaching hospital for the University of Texas Health Science Center at Houston from 2000 to 2008., Patients: Study patients were 5-14 years with postresuscitation Glasgow Coma Scale scores of 5-8., Interventions: The treatment group received 6 million autologous bone marrow-derived mononuclear cells/kg body weight IV within 48 hours of injury. The control group was treated in an identical fashion, per standard of care, guided by our traumatic brain injury management protocol, derived from American Association of Neurological Surgeons guidelines., Measurements and Main Results: The primary measure was the Pediatric Intensity Level of Therapy scale used to quantify treatment of elevated intracranial pressure. Secondary measures included the Pediatric Logistic Organ Dysfunction score and days of intracranial pressure monitoring as a surrogate for length of neurointensive care. A repeated-measure mixed model with marginal linear predictions identified a significant reduction in the Pediatric Intensity Level of Therapy score beginning at 24 hours posttreatment through week 1 (p < 0.05). This divergence was also reflected in the Pediatric Logistic Organ Dysfunction score following the first week. The duration of intracranial pressure monitoring was 8.2 ± 1.3 days in the treated group and 15.6 ± 3.5 days (p = 0.03) in the time-matched control group., Conclusions: IV autologous bone marrow-derived mononuclear cell therapy is associated with lower treatment intensity required to manage intracranial pressure, associated severity of organ injury, and duration of neurointensive care following severe traumatic brain injury. This may corroborate preclinical data that autologous bone marrow-derived mononuclear cell therapy attenuates the effects of inflammation in the early post-traumatic brain injury period.

Objective: To characterize membrane conductivity by applying mathematical modeling techniques and immunohistochemistry and to localize and predict areas of the bowel where aquaporins may be associated with edema resolution/prevention associated with hypertonic saline. Intestinal edema induced by resuscitation and mesenteric venous hypertension impairs intestinal transit/contractility. Hypertonic saline decreases intestinal edema and improves transit. Aquaporins are water transport membrane proteins that may be up-regulated with edema and/or hypertonic saline., Design: Laboratory study., Setting: University research laboratory., Subjects: Male Sprague Dawley rats, weighing 270 to 330 g., Interventions: Rats were randomized to control (with and without hypertonic saline) and mesenteric venous hypertension with either 80 mL/kg normal saline (RESUS + VH + VEH) or 80 mL/kg normal saline with hypertonic saline (RESUS + VH + HTS). After 6 hrs, intestinal wet/dry ratios, urine output, peritoneal fluid, and intraluminal fluid were measured. Hydraulic conductivity was calculated from our previously known and published pressure-flow data. The cDNA microarray, Western blot, polymerase chain reaction, and immunohistochemistry studies were conducted for candidate aquaporins and distribution in intestinal edema resolution., Measurements and Main Results: Hypertonic saline decreased edema and increased urine, intraluminal, and peritoneal fluid volume. RESUS + VH favors fluid flux into the interstitium. Hypertonic saline causes increased hydraulic conductivity at the seromuscular and mucosal surfaces at the same time limiting flow into the interstitium. This is associated with increased aquaporin 4 expression in the intestinal mucosa and submucosa., Conclusions: Hypertonic saline mitigates intestinal edema development and promotes fluid redistribution secondary to increased membrane conductivity at the mucosal and seromuscular surfaces. This is associated with up-regulation of aquaporin 4 gene expression and protein. Aquaporin 4 may be a useful therapeutic target for strategies to enhance edema resolution.

The purpose of this study is to determine the effect of clonidine on cardiac norepinephrine spillover utilizing an isolated rat heart preparation with attached cardiac sympathetic nerves. Following a 20-minute stabilization period, the sympathetic ganglion for each heart preparation was electrically stimulated with 10V and 2 Hz for 30 seconds (S1: 60 pulses). Heart rate, left ventricular developed pressure, and coronary perfusion pressure was allowed to return to baseline and the perfusate was randomly switched to Krebs buffer containing one of two treatments: placebo or clonidine (1 microM). After 10 minutes of treatment, the sympathetic ganglion was again electrically stimulated with 10V and 2 Hz for 30 seconds (S2: 60 pulses). The perfusate exiting the heart before, during, and after each electrical stimulation was collected for the determination of cardiac norepinephrine spillover. Clonidine administration significantly reduced cardiac norepinephrine spillover by approximately 50% (P < 0.05) and was associated with a 36% reduction in heart rate (P < 0.05). These findings provide evidence that clonidine can directly suppress NE spillover from cardiac sympathetic nerve terminals. Thus, suppression of cardiac NE by clonidine may be due to stimulation of presynaptic alpha2-adrenergic receptors or imidazoline subtype I receptors located on cardiac sympathetic nerve terminals. Results from our study demonstrate a reduction in cardiac NE spillover by clonidine and provide additional evidence that it can directly suppress peripheral sympathetic activity in that our results were obtained utilizing an isolated perfused heart preparation with attached cardiac sympathetic nerves devoid of any CNS input.