RESUMEN
We describe the case of a 30-year-old man who allegedly had a history of road traffic accidents. While walking on the road, he was hit by a truck. He presented with complaints of facial injuries and being unable to move his right lower limb. On examination, there is a 15x4 cm lacerated wound in the perineal area, with left testes exposed; anal tone could not be assessed; the right lower limb is externally rotated; and deformity is present with palpable peripheral pulses. He was diagnosed with a right sacral ala fracture, a distal one-third shaft of the right tibia fracture, and a right suprapubic rami fracture. Ultrasound of the right thigh showed hematoma and subcutaneous edema all around the gluteal and inguinal regions and fluid collection in the right inguinal region, which is suggestive of Morel-Lavallee lesion (MLL) type 6. On day two of admission, urine was dark in color, and creatinine kinase was elevated, which is suggestive of rhabdomyolysis. He was managed with hydration, electrolyte correction for rhabdomyolysis, and wound debridement for MLL apart from perineal injury, right sacral ala fracture, right suprapubic rami fracture, and distal one-third shaft of the right tibia fracture, with perineal repair and loop colostomy, pelvic binder, and external fixator, respectively. Early identification of the MLL associated with rhabdomyolysis in this polytrauma patient led to recovery and a successful outcome.
RESUMEN
Background In today's era of anesthesia, balanced anesthesia is the main basis of patient care and pain management. Of all the medications given during general anesthesia, premedication, induction agents, and muscle relaxants play a major role in keeping the hemodynamics properly under control. When laryngoscopy is performed to intubate, a pain stimulus will be generated, leading to a rise in blood pressure and heart rate. This stimulus can be avoided without any complications if appropriate premedication is given to the patient at the appropriate dosage. In this research, we compare the influence of injection esmolol and oral clonidine during the time of induction as premedications to suppress the hemodynamic response. Material and methods In a prospective randomized controlled trial, 90 patients were divided into three groups: Group E (esmolol) received 2 mg/kg IV esmolol diluted in 0.9% NS two minutes pre-anesthesia; Group C (clonidine) received oral clonidine 4 mcg/kg 90 minutes pre-anesthesia; and Group P (placebo) received IV normal saline and oral water. Blood pressure, heart rate, and mean arterial pressure were measured at baseline and seven subsequent time points. Results The study compared systolic blood pressure (SBP), mean arterial pressure (MAP), and diastolic blood pressure (DBP) changes over seven minutes in three groups, clonidine (Group C), placebo (Group P), and esmolol (Group E). At one minute, Group E showed a consistent MAP decrease from 95.21 mmHg to 85.92 mmHg, while Group C and Group P exhibited fluctuating trends. DBP decreased across all groups, with Group P ending highest (77.7 mmHg) and Group C lowest (66.8 mmHg). Group E's SBP decreased steadily from 126.2 mmHg to 118.0 mmHg, Group C decreased from 128 mmHg to 116.1 mmHg, and Group P showed more erratic fluctuations in SBP, DBP, and MAP. Conclusion These findings suggest that intravenous esmolol shows a good hemodynamic response having superior control over heart rate and getting the pressure under control quickly without major drop compared with the clonidine and placebo groups.
RESUMEN
OBJECTIVE: Granzyme A (GzmA) levels are elevated in the plasma and synovium of patients with rheumatoid arthritis (RA), suggesting involvement of this protease in the pathogenesis of the disease. GzmA contributes to sepsis by regulating the production of proinflammatory cytokines. The purpose of this study was to evaluate the contribution of GzmA to the pathogenesis of RA in vivo and to examine the possibility that GzmA acting via tumor necrosis factor (TNF) stimulates osteoclastogenesis. METHODS: Inflammatory arthritis induced by type II collagen was evaluated in wild-type, GzmA-deficient, and perforin-deficient mice. The osteoclastogenic potential of GzmA was examined in vitro using bone marrow cells and colony-forming unit-granulocyte-macrophage (CFU-GM) cells and in vivo using GzmA-deficient mice. RESULTS: Gene deletion of GzmA attenuated collagen-induced arthritis, including serum levels of proinflammatory cytokines, joint damage, and bone erosion in affected mice, suggesting that osteoclast activity is reduced in the absence of GzmA. Accordingly, GzmA-treated bone marrow cells produced multinucleated cells that fulfilled the criteria for mature osteoclasts: tartrate-resistant acid phosphatase (TRAP) activity, ß integrin expression, calcitonin receptor expression, and resorptive activity on dentin slices. GzmA appeared to act without accessory cells, and its activity was not affected by osteoprotegerin, suggesting a minor contribution of RANKL. It also induced the expression and secretion of TNF. Neutralization of TNF or stimulation of CFU-GM cells from TNF-/- mice prevented GzmA-induced osteoclastogenesis. GzmA-deficient mice had reduced osteoclastogenesis in vivo (fewer calcitonin receptor-positive multinucleated cells and fewer transcripts for cathepsin K, matrix metalloproteinase 9, and TRAP in joints) and reduced serum levels of C-terminal telopeptide of type I collagen. CONCLUSION: GzmA contributes to the joint destruction of RA partly by promoting osteoclast differentiation.
