Background: Postoperative pain after living donor hepatectomy is significant. Postoperative coagulopathy may limit the use of epidural analgesia, the gold standard for pain control in abdominal surgery. The erector spinae plane block (ESPB) is a novel regional anesthesia technique that has been shown to provide effective analgesia in abdominal surgery. In this study, we examined the effect of continuous ESPB, administered via catheters, on perioperative opioid requirements after right living donor hepatectomies for liver transplantation. Methods:We performed a retrospective cohort study in patients undergoing right living donor hepatectomy. Twenty-four patients who received preoperative ESPB were compared to 51 historical controls who did not receive regional anesthesia. The primary endpoint was the total amount of oral morphine equivalents (OMEs) required on the day of surgery and postoperative day (POD) 1. Results: Patients in the ESPB group required a lower total amount of OMEs on the day of surgery and POD 1 [141 (107-188) mg] compared the control group [293 (220-380) mg; P < .001]. Conclusions: The use of continuous ESPB significantly reduced opioid consumption following right living donor hepatectomy.

Assessment of kidney function is primarily based on urine output and Creatinine (Cr)-based methods to estimate glomerular filtration rate (GFR). The latter is confounded as Cr is not exclusively filtered by the kidney and rises relatively late after the onset of acute kidney injury (AKI). This leads to delays in recognition of reduced kidney function and diagnosis of AKI, particularly in critically ill patients where kidney function can change rapidly. The gold standard methods of GFR determination, such as inulin or iohexol clearance, are labor intensive and unfeasible in acute clinical settings. Proenkephalin A 119–159 (PENK) has been intensively studied as a novel biomarker of kidney function. PENK belongs to the enkephalin peptide family and is freely filtrated in the glomerulus. Plasma PENK concentration appears to correlate strongly with GFR. Moreover, increased plasma PENK concentrations are found to be associated with long-term kidney outcomes and mortality. In this review, we summarize the role of PENK in assessment of kidney function and its capacity to predict various clinical outcomes.

Background-Microvascular dysfunction and ischemia in muscle play a role in the development of cutaneous tactile allodynia in chronic post-ischemia pain (CPIP). Hence, studies were designed to assess whether pentoxifylline (PTX), a vasodilator and hemorrheologic agent, relieves allodynia in CPIP rats by alleviating microvascular dysfunction.Methods-Laser Doppler flowmetry of plantar blood flow was used to examine the effects of PTX on CPIP-induced alterations in post-occlusive reactive hyperemia (reflecting microvascular dysfunction), and von Frey testing was used to examine its effects on CPIP-induced allodynia. Time course effects of PTX on allodynia and microvascular dysfunction were assessed early (2-8 days) and late (18-25 days) post-ischemia/reperfusion (I/R) injury, and its effects on allodynia were also tested at 30 days post-I/R injury.Results-PTX (25 mg/kg) produced significant anti-allodynic effects throughout the 21-day time course, but was not effective 30 days post-IR injury. In laser Doppler studies, the reduced reactive hyperemia in early CPIP rats was significantly improved by PTX (25 mg/kg). Conversely, CIHR Author ManuscriptCIHR Author Manuscript CIHR Author Manuscript treatment with PTX at the same dose did not affect reactive hyperemia in late CPIP rats, likely since reactive hyperemia was not significantly reduced pre-drug in these animals.Conclusion-Since, poor tissue perfusion underlies early stages of CPIP pain, the ameliorative effect of PTX on microvascular dysfunction might account for its anti-allodynic effect in our experimental model of CRPS-I.

Background-Ischemia-reperfusion injury causes chronic postischemia pain (CPIP), and rats with higher glycemia during ischemia-reperfusion injury exhibit increased allodynia. Glycemiainduced elevation of nuclear factor kappa-B (NFκB) may contribute to increased allodynia.