SUMMARYIntroduction/Objective Subtrochanteric fractures are unstable, tending to a varus, antecurvatum, and shortening deformity. The aim of this paper was to compare operation time and fluoroscopy time between different internal fixation methods in the treatment of subtrochanteric fractures. Method The prospective study of the group of 27 patients with a subtrochanteric fracture treated by the SIF (selfdynamisable internal fixator with a trochanteric unit) method had been done. Operation time and fluoroscopy time values from this group were compared to the same parameters data from the literature for intramedullary (IM) nails, proximal femur locking plates (PF-LCP), dynamic condylar screws (DCS), and the 95°-angled blade plate. Results In the SIF group, operation time was 62.2 (25–140) minutes and fluoroscopy time was 43 (20–95) s. Average operation time from the literature data was: 102.1 (43–181) minutes for IM nail, 94.2 (75–129) minutes for PF-LCP, 105.3 (70–166) minutes for DCS and 221.5 (171–272) minutes for blade plate. Average fluoroscopy time from the literature data was: 109.6 (34–250) seconds for IM nail, 102.3 (47–180) seconds for PF-LCP, 238 seconds for DCS. Operation time and intraoperative fluoroscopy time were higher in IM nail, PF-LCP, DCS and blade plate comparing to SIF method (p < 0.05). Conclusion The above mentioned difference could be explained by a degree of required accuracy in the initial operative technique maneuvers, by used number of screws and by the type of the fracture reduction performance in different fixation methods. Operation time during IM nailing of subtrochanteric fractures sometimes can be shorter than average operation time in SIF method, what could be explained by the skill of the surgeon to perform as fast closed reduction for insertion of guide wire.
Abstract Respiratory failure is the predominant cause of death in humans and animals poisoned with anticholinesterases. Organophosphorus and carbamate anticholinesterases inhibit acetylcholinesterase irreversibly and reversibly, respectively. Some of them contain a quaternary atom that makes them lipophobic, limiting their action at the periphery, i.e. outside the central nervous system. They impair respiratory function primarily by inducing a desensitization block of nicotinic receptors in the neuromuscular synapse. Lipophilic anticholinesterases inhibit the acetylcholinesterase both in the brain and in other tissues, including respiratory muscles. Their doses needed for cessation of central respiratory drive are significantly less than doses needed for paralysis of the neuromuscular transmission. Antagonist of muscarinic receptors atropine blocks both the central and peripheral muscarinic receptors and effectively antagonizes the central respiratory depression produced by anticholinesterases. To manage the peripheral nicotinic receptor hyperstimulation phenomena, oximes as acetylcholinesterase reactivators are used. Addition of diazepam is useful for treatment of seizures, since they are cholinergic only in their initial phase and can contribute to the occurrence of central respiratory depression. Possible involvement of central nicotinic receptors as well as the other neurotransmitter systems – glutamatergic, opioidergic – necessitates further research of additional antidotes.
INTRODUCTION/AIM In acute organophosphate poisoning the issue of special concern is the appearance of muscle fasciculations and convulsions that cannot be adequately antagonised by the use of atropine and oxime therapy. The aim of this study was to examine atidotal effect of obidoxime or HI-6 combinations with memantine in mice poisoned with soman, dichlorvos or heptenophos. METHODS Male Albino mice were pretreated intravenously (iv) with increasing doses of oximes and/or memantine (10 mg/kg) at various times before poisoning with 1.3 LD-50 of soman, dichlorvos or heptenophos, in order to determine the median effective dose and the efficacy half-time. In a separate experiment, cerebral extravasation of Evans blue dye (40 mg/kg iv) was examined after application of memantine (10 mg/kg iv), midazolam (2.5 mg/kg intraperitonealy--ip) and ketamine (20 mg/kg ip) 5 minutes before soman (1 LD-50 subcutaneously--sc). RESULTS Coadministration of memantine induced a significant decrease in median effective dose in null time of both HI-6 (7.96 vs 1.79 gmoL/kg in soman poisoning) and obidoxime (16.80 vs 2.75 micromoL/kg in dichlorvos poisoning; 21.56 vs 6.63 micromoL/kg in heptenophos poisoning). Memantine and midazolam succeded to counteract the soman-induced proconvulsive activity. CONCLUSION Memantine potentiated the antidotal effect of HI-6 against a lethal dose of soman, as well as the ability of obidoxime to antagonize the toxic effects of dichlorvos and heptenophos probably partly due to its anticonvulsive properties.
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