Anesthetic Fluid Management of Patients With Hyponatremia Undergoing Living Donor Liver Transplantation.

OBJECTIVE: The objective of this study is to evaluate the changes in serum sodium levels in adult recipients with and without hyponatremia undergoing living donor liver transplantation (LDLT) without using hypertonic solution. METHODS: Patients were divided into 2 groups according to serum sodium level higher (GI) or lower (GII) than 130 mEq/L. The changes of serum sodium levels during an LDLT procedure and total sodium loads were compared between groups by using the Mann-Whitney U test, while the changes in the same group were paired by using the Student t test. A P value <.005 was considered significant. RESULTS: The total sodium load for GI (n = 438) and GII (n = 28) were 2737 ± 2159 mEq and 4017 ± 2830 mEq, respectively. Although GI received a significantly lower sodium load than GII, the serum sodium levels during the procedure were always within a normal range and higher than GII at all the measured time points; however, the changes of serum sodium level in GI from one point to the next measured point in the same group were unremarkable, while that of GII increased significantly between the 2 measured time points during the procedure. The mean total increase of serum sodium in GII was 5.57 ± 4.9 mEq/L in 14 hours of the LDLT procedure. None of the patients developed central pontine myelinosis (CPM) postoperatively. CONCLUSION: Patients with hyponatremia can be managed safely without using a hypertonic solution during liver transplantation. The mean increase of serum sodium of GII was of 5.57 ± 4.9 mEq/L, which was still within the acceptable and safe level. No postoperative CPM was observed in our GII patients.

Acute Kidney Injury in Adult Living Donor Liver Transplantation Performed with Different Methods of Inferior Vena Cava Clamping Maneuvers.

OBJECTIVE: The aim of this retrospective study is to evaluate and compare the incidence of acute kidney injury (AKI), defined as increase serum creatinine (SCr) of 0.3 mg/dl or increase in SCr to ≥1.5 times from baseline within 48 hour, in adult living donor liver transplantation patients performed with total cross clamp vs side clamp of the inferior vena cava (IVC). METHODS AND PATIENTS: Sixty adult living donor liver transplantation (LDLT) patients were divided into 2 groups: 30 patients in total IVC clamping (G1) and 30 in IVC side clamping (G2) during the anhepatic phase. Patients' characteristic, hemodynamic changes in percentage (%) as a result of different methods of IVC clamping, urine output during anhepatic phase were compared by using the Student t test, and the incidence of AKI were compared by using the χ2 test between groups. P value <.05 was regarded as significant. RESULTS: The negative impact of the 2 different ways of IVC clamping was significantly more severe in G1 compared to G2; consequently, the urine output of G1 was significantly less than G2. Although there was significantly more urine output of G2 during the anhepatic phase, the incidence of the postoperative AKI between groups was similar. CONCLUSION: The side clamp of the IVC had a significantly less negative impact on the hemodynamic parameters and provided sufficient urine output during the anhepatic phase (2.24 ± 3.17 vs 0.39 ± 0.33 mL/kg/h) compared to the total clamp of the IVC. But this favorable data did not protect the patient suffering from postoperative AKI in LDLT.

Comparison of Glucose Loads and Blood Glucose Changes in Patients With and Without Diabetes Mellitus Undergoing Living Donor Liver Transplantation.

BACKGROUND AND PURPOSE: The purpose of this study was to identify the quantitative amount of glucose load, which maintained the blood glucose levels between 100 and 180 mg/dL in patients with and without diabetes mellitus (DM) undergoing living donor liver transplantation (LDLT). METHODS AND PATIENTS: The anesthesia records of 477 adult LDLT patients were reviewed retrospectively. The total amount of glucose loads and the changes in blood glucose between groups were compared by using Mann-Whitney U test. One-year patient survival between groups was compared with Pearson's χ2 test. A P value of <.05 was considered statistically significant. RESULTS: Eighty patients diagnosed with DM, who were all type II except one, were placed in group 1 (G1); and 397 patients without DM were placed in group 2 (G2). Table 1 shows that G1 received significantly less glucose loads in comparison to G2, but all the measured blood glucose levels, except in the reperfusion phase, were significantly higher in G1 than in G2. Both groups received glucose loads of 0.342 ± 0.191 and 0.774 ± 0.191 mg/kg/min for G1 and G2, respectively. No difference in 1-year survival between groups was observed. CONCLUSION: Patients with DM required significantly lower glucose loads compared to patients without DM.

Combination therapy with extracorporeal shock wave and melatonin markedly attenuated neuropathic pain in rat.

This study tested the hypothesis that combination therapy using extracorporeal shock wave (ECSW)-melatonin (Mel) was superior to either alone at ameliorating neuropathic pain (NP). NP was induced by chronic constriction injury (CCI) to the left sciatic nerve in rats. Animals were categorized into sham control (group 1), CCI only (group 2), CCI-ECSW (group 3), CCI-Mel (group 4) and CCI-ECSW-Mel (group 5). By days 2 and 8 after CCI, the mechanical paw withdrawal threshold (MPWT)/thermal paw withdrawal latency (TPWL) were highest in group 2, lowest in group 1, significantly lower in group 5 than in groups 3 and 4 (all p<0.0001), and not significantly different between groups 3 and 4. The protein expressions of inflammatory (TNF-α/NF-κB/MMP-9/IL-1ß/GFAP/ox42), oxidative-stress (NOX-1/NOX-2/NOX-4/oxidized protein), DNA/mitochondrial-damaged (γ-H2AX/cytosolic mitochondria), apoptotic (cleaved capase-3/PARP), and MAPK family biomarkers (p-P38/p-JNK/p-ERK1/2) in dorsal root ganglia and spinal dorsal horn expressed a similar pattern of MPWT/TPWL among the five groups, except for significantly higher in group 4 than in group 3 (all p<0.0001). The protein expressions of Nav.1.3, Nav.1.8 and Nav.1.9 in sciatic nerve displayed an identical pattern to inflammation among the five groups (all p<0.001). Pain facilitated cellular expressions (p-P38+/peripherin+ cells, P38+/NF200+ cells) displayed an identical pattern to inflammation among the five groups (all p<0.0001). In conclusion, ECSW-Mel combination therapy markedly ameliorated NP induced by CCI.

Pulsed Radiofrequency Attenuates Complete Freund's Adjuvant-Induced Epigenetic Suppression of Potassium Chloride Cotransporter 2 Expression.

Background: Pulsed radiofrequency (PRF) treatment offers pain relief for patients suffering from chronic pain who do not respond well to conventional treatments. We tested whether PRF treatment attenuated complete Freund's adjuvant (CFA)-induced inflammatory pain. Epigenetic modification of potassium-chloride cotransporter 2 (KCC2) gene expression was examined to elucidate the potential contributing mechanism. Methods: Male Sprague-Dawley rats were injected with CFA into the plantar surface of the left hind paw to induce inflammation. PRF (20 minutes of 500-kHz RF pulses, delivered at a rate of 2 Hz, maximum temperature 42ºC) was delivered to the L5 and L6 anterior primary ramus just distal to the intervertebral foramen of adult CFA or saline rats. The hind paw withdrawal threshold to von Frey filament stimuli and withdrawal latency to radiant heat were determined before and after CFA. Acetyl-histone H3 and H4 was determined by chromatin immunoprecipitation in spinal dorsal horn. KCC2 expression was determined by Western blot. Inhibitory synaptic function was evaluated by patch clamp in lamina II neurons. Results: KCC2 gene expression was suppressed through histone hypoacetylation, resulting in decreased efficacy of GABAergic signaling in CFA rats. PRF increased histone acetylation and KCC2 expression, partially restored the GABA synaptic function, and relieved sensitized pain behavior. Conclusion: These findings suggest that PRF might be an alternative therapy for inflammatory pain. One of the underlying mechanisms is through modification of KCC2, which is an important determinant for the efficacy of inhibitory neurotransmission in the spinal cord, and its expression levels are regulated by histone acetylation epigenetically following inflammation.

Reduction of spinal glycine receptor-mediated miniature inhibitory postsynaptic currents in streptozotocin-induced diabetic neuropathic pain.

Diabetic neuropathic pain (DNP) is a common clinical problem, and the mechanisms underlying the onset and progression of this complication are poorly understood. The present study examined the glycine receptors (GlyR) in the control of synaptic input to dorsal horn neurons in diabetes. Male Sprague-Dawley rats with or without streptozotocin (STZ) intraperitoneal injections were used. Tactile sensitivities were assessed by measuring paw withdrawal thresholds to von Frey filaments for four weeks. The extent of GlyR-mediated inhibition controlling primary afferent-evoked excitation in dorsal horn neurons was examined by using the whole cell patch clamp recording technique in isolated adult rat spinal cord slices. The content of the spinal dorsal horn glycine levels was measured by microdialysis. An intrathecal glycine agonist injection was used to test whether mimicking endogenous glycine-receptor-mediated inhibition reduces DNP. We found that persistent hyperglycemia induced by the administration of STZ caused a decrease in the paw withdrawal latency to mechanical stimuli. The miniature inhibitory post-synaptic current (mIPSC) rise, decay kinetics and mean GlyR-mediated mIPSC amplitude were not affected in DNP. The mean frequency of GlyR-mediated mIPSC of lamina I neurons from DNP rats was, however, significantly reduced when compared with neurons from control rats. Principal passive and active membrane properties and the firing patterns of spinal lamina I neurons were not changed in DNP rats. Spinal microdialysis rats had a significantly decreased glycine level following its initial elevation. The intrathecal administration of glycine diminished tactile pain hypersensitivity in DNP rats. In conclusion, these results indicate that long-lasting hyperglycemia induced by STZ injections leads to a reduced glycinergic inhibitory control of spinal lamina I neurons through a presynaptic mechanism.