Effect and Outcome of Intraoperative Fluid Restriction in Living Liver Donor Hepatectomy.

BACKGROUND The purpose of this study was to evaluate the effect and outcome of intraoperative fluid restriction in living liver donor hepatectomy, regarding changes in intraoperative CVP levels, blood loss, and postoperative renal function. MATERIAL AND METHODS The charts of 167 patients were reviewed and analyzed retrospectively. Intraoperative central venous pressure levels, blood loss, fluids infused, and urine output per hour, before and after the liver allograft procurement, were calculated. Perioperative renal functions were also analyzed. RESULTS Fluid infused before and after liver allograft procurement was 3.21±1.5 and 9.0±3.9 mL/Kg/h and urine output was 1.5±0.7 and 1.8±1.4 mL/Kg/h, respectively. Intraoperative estimated blood loss was 91.3±78.9 mL. No patients required blood transfusion. Their preoperative and postoperative hemoglobin were 12.3±2.7 and 11.7±1.7 g/dL. CVP levels decreased gradually from 10.4±3.0 to a low of 8.1±1.9 mmHg at the time of transection of the liver parenchyma. Renal functions were not significantly affected based on the determination of BUN and creatinine levels. CONCLUSIONS The methods used to lower CVP are moderate and slow, with 2 main goals achieved: minimal blood loss (91.3±78.9 ml) and no blood transfusion. Furthermore, it did not have any negative effect on renal function.

Clinical Beneficial Effects of Using Crystalloid only in Recipients of Living Donor Liver Transplantation.

OBJECTIVE: Liver transplantation (LT) is a major surgery associated with intraoperative massive fluid shift, which is usually replaced by crystalloid, 5% albumin (colloid) and blood products. We studied 15 patients from 477 consecutive recipients of adult living donor liver transplantation. Each patient received crystalloid only during LT. Whether LT provides any clinical benefit is not clear and must be determined. METHODS AND PATIENTS: The anesthesia records of 477 adult LDLT were reviewed retrospectively. The patients were divided into three groups according to the fluids received. Group I (GI) had received blood products, 5% albumin and crystalloid, group II (GII) received 5% albumin and crystalloid, and group III (GIII) received crystalloid only. The characteristic intraoperative variable and postoperative acute rejection and survival rate were compared amongst groups by using One Way ANOVA post hoc with Bonferroni and by Ficher's Exact test and Chi-square χ² test. RESULTS AND CONCLUSIONS: GIII had less intraoperative ascites and blood loss; they also had more stable hemodynamics. Furthermore, they could be extubated significantly earlier than GI, and the one- and three-year survival rates were excellent, with 100% in GIII, while that of GI and GII were 94.1%, 90.5% and 98.6%, 94.5%, respectively.

GADD45A protects against cell death in dorsal root ganglion neurons following peripheral nerve injury.

A significant loss of neurons in the dorsal root ganglia (DRG) has been reported in animal models of peripheral nerve injury. Neonatal sensory neurons are more susceptible than adult neurons to axotomy- or nerve growth factor (NGF) withdrawal-induced cell death. To develop therapies for preventing irreversible sensory cell loss, it is essential to understand the molecular mechanisms responsible for DRG cell death and survival. Here we describe how the expression of the growth arrest- and DNA damage-inducible gene 45α (GADD45A) is correlated with neuronal survival after axotomy in vivo and after NGF withdrawal in vitro. GADD45A expression is low at birth and does not change significantly after spinal nerve ligation (SNL). In contrast, GADD45A is robustly up-regulated in the adult rat DRG 24 hr after SNL, and this up-regulation persists as long as the injured fibers are prevented from regenerating. In vitro delivery of GADD45A protects neonatal rat DRG neurons from NGF withdrawal-induced cytochrome c release and cell death. In addition, in vivo knockdown of GADD45A expression in adult injured DRG by small hairpin RNA increased cell death. Our results indicate that GADD45A protects neuronal cells from SNL-induced cell death.