RESUMO
Laparoscopic cholecystectomy is a common general surgery procedure, with over a million laparoscopic cholecystectomies performed in the United States annually. A rare presentation, which may be encountered incidentally during surgery, is torsion of the gallbladder. Gallbladder torsion is encountered in 0.01% of all patients with acute cholecystitis. It should be considered in the differential diagnosis of elderly female patients presenting with symptoms of acute or chronic cholecystitis. In this case report, we discuss the incidental finding of gallbladder torsion during laparoscopic cholecystectomy in an 82-year-old female admitted to the hospital with symptoms of cholecystitis. Preoperative CT imaging revealed a chronic, large hiatal hernia and a dilated gallbladder containing heterogeneous densities, possibly related to sludge. During the operation, a necrotic, torsed gallbladder and long cystic duct were found. A laparoscopic cholecystectomy was performed and the remainder of the patient's hospital course was uncomplicated. Intraoperatively, our patient was found to have torsion of the gallbladder. Preoperative lab values revealed mild hyponatremia, hypokalemia, and hypochloremia with normal liver enzymes, bilirubin, and alkaline phosphatase levels. This is consistent with documented cases, as typically the biliary tree is not obstructed. Additionally, preoperative imaging rarely reveals the diagnosis. Prompt detorsion and cholecystectomy should be performed to prevent gangrene and perforation. Gallbladder torsion can result in perforation if not quickly identified and treated. We recommend prompt laparoscopic detorsion and cholecystectomy to prevent perforation.
RESUMO
[This corrects the article DOI: 10.3389/fncir.2018.00028.].
RESUMO
After injury to the corticospinal tract (CST) in early development there is large-scale adaptation of descending motor pathways. Some studies suggest the uninjured hemisphere controls the impaired forelimb, while others suggest that the injured hemisphere does; these pathways have never been compared directly. We tested the contribution of each motor cortex to the recovery forelimb function after neonatal injury of the CST. We cut the left pyramid (pyramidotomy) of postnatal day 7 rats, which caused a measurable impairment of the right forelimb. We used pharmacological inactivation of each motor cortex to test its contribution to a skilled reach and supination task. Rats with neonatal pyramidotomy were further impaired by inactivation of motor cortex in both the injured and the uninjured hemispheres, while the forelimb of uninjured rats was impaired only from the contralateral motor cortex. Thus, inactivation demonstrated motor control from each motor cortex. In contrast, physiological and anatomical interrogation of these pathways support adaptations only in the uninjured hemisphere. Intracortical microstimulation of motor cortex in the uninjured hemisphere of rats with neonatal pyramidotomy produced responses from both forelimbs, while stimulation of the injured hemisphere did not elicit responses from either forelimb. Both anterograde and retrograde tracers were used to label corticofugal pathways. There was no increased plasticity from the injured hemisphere, either from cortex to the red nucleus or the red nucleus to the spinal cord. In contrast, there were very strong CST connections to both halves of the spinal cord from the uninjured motor cortex. Retrograde tracing produced maps of each forelimb within the uninjured hemisphere, and these were partly segregated. This suggests that the uninjured hemisphere may encode separate control of the unimpaired and the impaired forelimbs of rats with neonatal pyramidotomy.