Successful intrathecal neurolytic block for the management of cancer pain in a 10-year-old child: a case report.

BACKGROUND: Cancer pain management in children is challenging owing to their unique patient characteristics. We present the case of a 10-year-old girl whose cancer pain was successfully managed using an intrathecal neurolytic block. CASE PRESENTATION: The patient experienced severe cancer pain due to recurrent right ilium osteosarcoma. The tumor progressed rapidly despite chemoradiotherapy and gradually invaded the right lumbar plexus, which resulted in severe neuropathic pain in the right lower extremity. Systemic analgesics failed to attenuate the pain. We performed an intrathecal neurolytic block using 10% phenol-glycerol. The neurolytic block completely relieved her right lower extremity pain. After the block, the patient's quality of life improved, and she spent her time with family. CONCLUSIONS: The intrathecal neurolytic block successfully relieved the patient's cancer pain. Successful intrathecal neurolytic blocks require meticulous pain assessment of individual patients, to avoid possible serious complications such as paresis/paralysis and bladder/bowel dysfunction.

Effects of dexmedetomidine on lipopolysaccharide-induced acute kidney injury in rats and mitochondrial function in cell culture.

PURPOSE: To investigate the mechanisms through which dexmedetomidine (DEX) could improve the renal injury in lipopolysaccharide (LPS)-induced acute kidney injury (AKI) and examine how TNF-α or DEX might affect mitochondrial function and renal injury. METHODS: In vivo experiments involved 24 rats randomly allocated to a sham group, an LPS group, and an LPS + DEX group. Serum creatinine, lactate, TNF-α, IL-1ß, and IL-6 concentrations, as well as urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels, were measured 0, 3, and 6 h after the start of the experiments. Histopathological examinations were performed to determine the extent of LPS-induced renal injury and recovery by administration of DEX. in vitro, human embryonic kidney 293 cells were treated with or without (control) several concentrations of TNF-α and DEX for 24 h before measurements of the oxygen consumption rate (OCR) under basal conditions and with the addition of oligomycin, carbonylcyanide-p-trifluoromethoxyphenylhydrazone, antimycin A, and rotenone, as well as intracellular reactive oxygen species (ROS) levels. RESULTS: DEX attenuated LPS-induced increases in serum creatinine and IL-6 concentrations. LPS administration caused histological tissue damage in the kidney, but DEX prevented such damage. In vitro, DEX suppressed TNF-α-induced increases in basal OCR and ROS levels and inhibited decreases of ATP production induced by TNF-α. CONCLUSION: DEX has protective effects for cells and tissues of the kidney by inhibiting oxygen consumption and hypoxia or by improving mitochondrial dysfunction via TNF-α in the renal cells. These results might point to DEX being an important new therapeutic target for the treatment of septic AKI.

Effects of Landiolol in Lipopolysaccharide-Induced Acute Kidney Injury in Rats and In Vitro.

The mechanisms by which landiolol, an ultra-short-acting, selective ß-1 blocker, could improve septic acute kidney injury and how inflammation might affect mitochondrial function and cause the renal injury were examined. Male Wistar rats (250 g-300 g) were randomly allocated to three groups: a sham control group (n = 8); a lipopolysaccharide (LPS) group (n = 8); and an LPS + landiolol group (n = 8). LPS was administered intravenously at the start of the experiments; the LPS + landiolol group rats received LPS and continuous intravenous landiolol. Serum creatinine and lactate concentrations and hemodynamic parameters were measured 3 and 6 h after the experiments started. TNF-α, IL-1ß, and IL-6 levels and urinary 8-OHdG concentrations were determined. The extent of LPS-induced renal injury and recovery with landiolol were examined histopathologically. Metabolic analysis in human embryonic kidney cells was performed using Seahorse analysis. The effects of landiolol on cytokine-induced mitochondrial stress and glycolytic stress were examined. Treatment with landiolol was shown to normalize serum creatinine and lactate levels following intravenous LPS administration (Cr: LPS group 0.8 ±â€Š0.6 mg/mL, LPS + landiolol group 0.5 ±â€Š0.1 mg/mL; P < 0.05). In the in vitro experiments, TNF-α induced an increase in mitochondrial oxygen consumption, which was attenuated by landiolol, which could represent a mechanism for renal protection. Landiolol may have protective effects on the cells and tissues of the kidney by inhibiting oxygen consumption and hypoxia caused by TNF-α in renal cells. These results suggest that landiolol may be an important new therapeutic target for treating inflammation-associated kidney injury.