Impact of Isolyte Versus 0.9% Saline on Postoperative Event of Acute Kidney Injury Assayed by Urinary [TIMP-2] × [IGFBP7] in Patients Undergoing Cardiac Surgery.

OBJECTIVE: Administration of excess chloride in 0.9% normal saline (NS) decreases renal perfusion and glomerular filtration rate, thereby increasing the risk for acute kidney injury (AKI). In this study, the effect of NS versus Isolyte use during cardiac surgery on urinary levels of tissue inhibitor of metalloproteinase 2 and insulin-like growth factor-binding protein 7 [TIMP-2] × [IGFBP7] and postoperative risk of AKI were examined. DESIGN: Prospective, randomized, and single-blinded trial. SETTING: Single university medical center. PARTICIPANTS: Thirty patients over 18 years without chronic renal insufficiency or recent AKI undergoing elective cardiac surgery. INTERVENTIONS: Subjects were randomized to receive either NS or Isolyte during the intraoperative period. MEASUREMENTS AND MAIN RESULTS: The primary outcome was the change in urinary levels of [TIMP2] × [IGFBP7] from before surgery to 24 hours postoperatively. Secondary outcomes included serum creatinine pre- and postoperatively at 24 and 48 hours, serum chloride pre- and postoperatively at 24 and 48 hours, need for dialysis prior to discharge, and arterial pH measured 24 hours postoperatively. Sixteen patients received NS and 14 patients received Isolyte. Three patients developed AKI within the first 3 postoperative days, all in the NS group. The authors found increases in [TIMP-2] × [IGFBP7] in both groups. However, the difference in this increase between study arms was not significant (p = 0.92; -0.097 to 0.107). CONCLUSION: The authors observed no change in urinary [TIMP-] × [IGFBP7] levels in patients receiving NS versus Isolyte during cardiac surgery. Future larger studies in patients at higher risk for AKI are recommended to evaluate the impact of high- versus lower-chloride solutions on the risk of postoperative AKI after cardiac surgery.

Quantification of partial or complete A4 pulley release with FDP repair in cadaveric tendons.

PURPOSE: Repair of a lacerated flexor digitorum profundus (FDP) tendon underneath or just distal to the A4 pulley can be technically challenging, and success can be confounded by tendon triggering and scarring to the pulley. The purpose of this study was to quantify the effect of partial and complete A4 pulley release in the context of a lacerated and repaired FDP tendon just distal to the A4 pulley. METHODS: Tendon biomechanics were tested in 6 cadaveric hands secured to a rigid frame, permitting measurement of tendon excursion, tendon force, and finger range of motion. After control testing, each finger had laceration and repair of the FDP tendon at the distal margin of the A4 pulley using a 6-strand core suture technique and epitendinous repair. Testing was then repeated after the following interventions: (1) intact A4 pulley, (2) release of the distal half of the A4 pulley, (3) complete release of the A4 pulley, and (4) continued proximal release of the sheath to the distal edge of A2 (release of C2, A3, and C1 pulleys). Release of the pulleys was performed by incision; no tissue was removed from the specimens. RESULTS: From full extension to full flexion, average FDP tendon excursion for all intact digits was 37.9 ± 1.5 mm, and tendon repair resulted in average tendon shortening of 1.6 ± 0.4 mm. Flexion lag increased from <1 mm to >4 mm with venting of the A4 pulley, complete A4 release, and proximal sheath release, respectively. Compared to the intact state, repair of the tendon with an intact A4 pulley, release of half the A4 pulley, complete A4 release, and proximal sheath release resulted in percentage increases in work of flexion of 11.5 ± 3.1%, 0.83 ± 2.8%, 2.6 ± 2.4%, and 3.25 ± 2.2%, respectively. CONCLUSIONS: After FDP laceration and repair in the region of the A4 pulley, work of flexion did not increase by more than 3% from control conditions after partial or complete A4 pulley release, and work of flexion was significantly less than that achieved by performing a repair and leaving the A4 pulley intact.

Effects of risperidone on locomotor activity and spatial memory in rats with hippocampal damage.

Hippocampal damage produces spatial memory impairment and hyperactivity in animals, while reductions in hippocampal size have been associated with memory deficits in humans. There are no known treatments for the behavioral changes specifically related to reduced hippocampal size. The purpose of this study was to determine if risperidone, an atypical antipsychotic drug that has shown cognitive-enhancing properties in animals and humans, could alleviate the behavioral disturbances produced by hippocampal damage in rats. Young adult male Sprague-Dawley rats received either sham stereotaxic surgery or direct stereotaxic infusions of N-methyl-d-aspartate (NMDA) into the dorsal hippocampus to produce hippocampal damage. One week later, animals in each group received daily subcutaneous injections of either saline or risperidone (0.2mg/kg) until the end of the experiment. Three weeks after surgery, locomotor activity was tested in all animals. During the fourth and fifth post-surgical weeks, animals were tested in a discrete-trial, delayed rewarded alternation memory paradigm. Risperidone reversed lesion-induced hyperactivity; however it also decreased activity in the sham control rats. In the delayed alternation task, there were significant drug and lesion effects irrespective of the day of testing, but there was no drugxlesion interaction. Hippocampal lesions impaired performance in the delayed alternation task in saline and risperidone-treated rats. However, risperidone modestly improved performance in lesioned and sham controls in comparison to saline-treated lesioned and sham controls. Risperidone also slowed choice time in the alternation task. These data indicate that risperidone does not specifically correct the neurobiological consequences of hippocampal damage, but that animals with hippocampal damage nonetheless maintain a significant degree of sensitivity to the beneficial effects of risperidone.