Transient Acute Diplopia as a Rare Side Effect of Hydromorphone: A Case Report.

Diplopia, or double vision, has been listed as a rare adverse effect of intravenous hydromorphone, although there are no case studies or literature documenting this. We detail a case of acute transient diplopia correlated with the use of intraoperative hydromorphone and postoperative hydromorphone patient-controlled analgesia. Although the mechanism for this adverse effect is unknown, there may be risk factors that predispose patients to the potential toxic metabolic effects of hydromorphone. We share the first published case of diplopia as a clinically relevant adverse effect of hydromorphone and propose a potential reason behind this association.

The Effect of Preoperative Renal Failure on Outcomes Following Infrainguinal Endovascular Interventions for Peripheral Arterial Disease.

PURPOSE: To analyze the effect of a patient's renal failure status on acute outcomes after lower extremity endovascular interventions for peripheral artery disease. MATERIALS AND METHODS: A retrospective analysis of the American College of Surgery National Surgical Quality Improvement Program database from 2014 to 2017 was conducted. Patients were included based on current procedural terminology codes. They were divided into renal failure cohorts. Six thousand seven hundred and sixty-five patients were included in the analysis, 11.0% of whom had renal failure. A univariate analysis was performed using chi-squared test or Fischer's exact test as appropriate. Multivariate logistic regression models were constructed, while controlling for relevant patient factors, to identify the effect of renal failure on several outcomes of interest after the intervention. A sensitivity analysis was performed with a propensity score-matched cohort. RESULTS: Patients with renal failure were more likely to have infrapopliteal interventions (38.0% vs 20.9%), critical limb ischemia with tissue loss (73.5% vs 38.9%), diabetes (70.9% vs 52.3%), preoperative wound infection (59.2% vs 30.7%), mortality (5.1% vs 1.3%), prolonged hospital stay (68.5% vs 46.5%), transfusion after the intervention (13.3% vs 9.1%), reoperation (18.3% vs 9.5%), and readmission (24.9% vs 12.6%), compared to patients without renal failure. The multivariate analysis found renal failure to be significant for mortality (odds ratio [OR] = 4.11, 95% confidence interval [CI] = 2.71-6.24), any complication (OR = 2.03, 95% CI = 1.72-2.39), extended length of stay (OR = 1.53, 95% CI = 1.28-1.83), sepsis (OR = 2.37, 95% CI = 1.60-3.51), readmission (OR = 1.89, 95% CI = 1.57-2.29), reoperation (OR = 1.84, 95% CI = 1.48-2.27), major adverse cardiovascular event (OR = 3.50, 95% CI = 2.54-4.84), and major adverse limb event (OR = 1.97, 95% CI = 1.55-2.51). P value was <.001 unless otherwise noted. CONCLUSIONS: Renal failure before the intervention places patients at a significantly elevated risk of morbidity and mortality following endovascular revascularization procedures for peripheral artery disease.

Persistent acidosis after reperfusion-A prognostic indicator of increased 30-day and in-hospital postoperative mortality in liver transplant recipients.

During liver transplantation, the patient is at risk of developing progressive lactic acidosis. Following reperfusion, correction of acidosis may occur. In some patients, acidosis will worsen, a phenomenon referred to as persistent acidosis after reperfusion (PAAR). We compared postoperative outcomes in patients who manifested PAAR vs those that did not. All adult patients undergoing liver transplantation from 2002 to 2015 were included. PAAR is defined by the presence of a significant negative slope coefficient for base excess values measured after hepatic artery anastomosis through 72 hours postoperatively. Primary outcome was a composite of 30-day and in-hospital mortality. Secondary outcomes included: ICU LOS, total hospital LOS, and re-transplantation rate within 7 days. PAAR occurred in 10% of the transplant recipients. Patients with PAAR had higher MELD, BMI, and eGFR and demonstrated a longer median ICU LOS and hospital median LOS with a trend toward mortality difference. But, after propensity matching, the mortality rate difference became significantly higher in patients with PAAR compared with matched controls while the ICU LOS differences disappeared. The re-transplantation rates were similar also between the PAAR and no PAAR groups. The cohort with PAAR had a significant 30-day and in-hospital increase in mortality after propensity score matching.

Elevated sensitivity of macrosteatotic hepatocytes to hypoxia/reoxygenation stress is reversed by a novel defatting protocol.

Macrosteatotic livers exhibit elevated intrahepatic triglyceride (TG) levels in the form of large lipid droplets (LDs), reduced adenosine triphosphate (ATP) levels, and elevated reactive oxygen species (ROS) levels, and this contributes to their elevated sensitivity to ischemia/reperfusion injury during transplantation. Reducing macrosteatosis in living donors through dieting has been shown to improve transplant outcomes. Accomplishing the same feat for deceased donor grafts would require ex vivo exposure to potent defatting agents. Here we used a rat hepatocyte culture system exhibiting a macrosteatotic LD morphology, elevated TG levels, and an elevated sensitivity to hypoxia/reoxygenation (H/R) to test for such agents and ameliorate H/R sensitivity. Macrosteatotic hepatocyte preconditioning for 48 hours with a defatting cocktail that was previously developed to promote TG catabolism reduced the number of macrosteatotic LDs and intracellular TG levels by 82% and 27%, respectively, but it did not ameliorate sensitivity to H/R. Supplementation of this cocktail with l-carnitine, together with hyperoxic exposure, yielded a similar reduction in the number of macrosteatotic LDs and a 57% reduction in intrahepatic TG storage, likely by increasing the supply of acetyl coenzyme A to mitochondria, as indicated by a 70% increase in ketone body secretion. Furthermore, this treatment reduced ROS levels by 32%, increased ATP levels by 27% (to levels near those of lean controls), and completely abolished H/R sensitivity as indicated by approximately 85% viability after H/R and the reduction of cytosolic lactate dehydrogenase release to levels seen in lean controls. Cultures maintained for 48 hours after H/R were approximately 83% viable and exhibited superior urea secretion and bile canalicular transport in comparison with untreated macrosteatotic cultures. In conclusion, these findings show that the elevated sensitivity of macrosteatotic hepatocytes to H/R can be overcome by defatting agents, and they suggest a possible route for the recovery of discarded macrosteatotic grafts.