. Pyruvate improves redox status and decreases indicators of hepatic apoptosis during hemorrhagic shock in swine. Am J Physiol Heart Circ Physiol 283: H1634-H1644, 2002. First published June 20, 2002 10.1152/ ajpheart.01073.2001.-Previous studies have shown that the liver is the first organ to display signs of injury during hemorrhagic shock. We examined the mechanism by which pyruvate can prevent liver damage during hemorrhagic shock in swine anesthetized with halothane. Thirty minutes after the induction of a 240-min controlled arterial hemorrhage targeted at 40 mmHg, hypertonic sodium pyruvate (0.5 g ⅐ kg Ϫ1 ⅐ h Ϫ1 ) was infused to achieve an arterial concentration of 5 mM. The volume and osmolality effects of pyruvate were matched with 10% saline (HTS) and 0.9% saline (NS). Although the peak hemorrhage volume increased significantly in both the pyruvate and HTS group, only the pyruvate treatment was effective in delaying cardiovascular decompensation. In addition, pyruvate effectively maintained the NADH/NAD redox state, as evidenced by increased microdialysate pyruvate levels and a significantly lower lactateto-pyruvate ratio. Pyruvate also prevented the loss of intracellular antioxidants (GSH) and a reduction in the GSH-to-GSSG ratio. These beneficial effects on the redox environment decreased hepatic cellular death by apoptosis. Pyruvate significantly increased the ratio of Bcl-Xl (antiapoptotic molecule)/Bax (proapoptotic molecule), prevented the release of cytochrome c from mitochondria, and decreased the fragmentation of caspase 3 and poly(ADP ribose) polymerase (DNA repair enzyme). These beneficial findings indicate that pyruvate infused 30 min after the onset of severe hemorrhagic shock is effective in maintaining the redox environment, preventing the loss of the key antioxidant GSH, and decreasing early apoptosis indicators. glutathione; redox state; caspases DESPITE ADVANCES IN THE EARLY CARE of trauma victims over the past two decades, multiple organ failure (MOF) continues to be a major factor in the morbidity and mortality that occurs after resuscitation from hemorrhagic shock (16). While there are numerous factors that influence the development of MOF, there is increasing evidence that hepatic dysfunction plays a central role (21,24,42,43). Experimental studies have shown that despite acute aggressive resuscitation, there is a consistent depression in microvascular blood flow that results in hypoperfusion and progressive hepatic dysfunction (32,42,43). This suggests that despite the restoration of global oxygen delivery, additional pharmacological therapies are needed to prevent or reverse ongoing hepatotoxicity. However, the precise mechanisms of hepatocellular dysfunction after severe hemorrhagic shock are not well defined. Some investigators have shown that the reduction in immunological mediators, such as tumor necrosis factor-␣, improves outcome indicators (23,41). Others have shown that there is severe hepatic energy depletion during hemorrhagic shock and that improvement in the hepatoce...

Purpose: Coronavirus disease 2019 (COVID-19) is associated with hypercoagulability and increased thrombotic risk. The impact of prehospital antiplatelet therapy on inhospital mortality is uncertain. Methods:This was an observational cohort study of 34 675 patients ≥50 years old from 90 health systems in the United States. Patients were hospitalized with laboratory-confirmed COVID-19 between February 2020 and September 2020. For all patients, the propensity to receive prehospital antiplatelet therapy was calculated using demographics and comorbidities. Patients were matched based on propensity scores, and in-hospital mortality was compared between the antiplatelet and nonantiplatelet groups. Results:The propensity score-matched cohort of 17 347 patients comprised of 6781 and 10 566 patients in the antiplatelet and non-antiplatelet therapy groups, respectively. In-hospital mortality was significantly lower in patients receiving prehospital antiplatelet therapy (18.9% vs. 21.5%, p < .001), resulting in a 2.6% absolute reduction in mortality (HR: 0.81, 95% CI: 0.76-0.87, p < .005). On average, 39 patients needed to be treated to prevent one in-hospital death. In the antiplatelet therapy group, there was a significantly lower rate of pulmonary embolism (2.2% vs. 3.0%, p = .002) and higher rate of epistaxis (0.9% vs. 0.4%, p < .001). There was no difference in the rate of other hemorrhagic or thrombotic complications. Conclusions:In the largest observational study to date of prehospital antiplatelet therapy in patients with COVID-19, there was an association with significantly lower in-hospital mortality. Randomized controlled trials in diverse patient populations with | 2815 CHOW et al.

This cohort study investigates whether early aspirin use is associated with lower 28-day in-hospital mortality among patients with moderate COVID-19.

Epidural analgesia is a widely used method of pain control in the labor and delivery setting but is not without risks. We present a case of Horner's syndrome and trigeminal nerve palsy as a rare complication of epidural analgesia in an obstetric patient. Although reported in few instances in the anesthesia literature, awareness among providers in obstetrics is critical because this could be the first sign of a high sympathetic blockade resulting in potential maternal-fetal morbidity. Case ReportA healthy 25-year-old woman, gravida 2 para 1, was admitted to the hospital for active labor at 39 weeks gestation. Her past medical history was remarkable only for occasional migraine headaches, and her prenatal course, including labs, had been unremarkable. During an uneventful first stage of labor, epidural anesthesia was requested. A lumbar epidural catheter was placed at the interspace between the third and fourth lumbar vertebrae using a midline approach and a loss of resistance to saline through a 17-gauge Touhy needle. A test dose of 3 mL of 1.5% lidocaine with 5 g of epinephrine per milliliter was administered without appreciable evidence of either intravascular or intrathecal placement of the catheter. A bolus of 10 mL of 0.2% bupivacaine with 2 g of fentanyl per milliliter was administered over 10 minutes, and then an infusion of the same solution was started at 8 mL per hour. Approximately 20 minutes after epidural catheter placement, the patient complained that the left side of her face "felt funny." On evaluation by her family physician, the patient reported decreased sensation to light touch on the left cheek in the distribution of the maxillary branch of the trigeminal nerve and was observed to have miosis and ptosis on the left side. Pinprick demonstrated the level of analgesia at the fourth thoracic segment on the left and at the fifth thoracic segment on the right. The patient's grip strength was found to be normal, and she denied dyspnea. There were no other cranial nerve abnormalities or neurologic deficits appreciated.Simultaneously, the patient's blood pressure dropped from 115/68 mm Hg to a range of 90s/30s mm Hg for several minutes. After receiving 10 mg of ephedrine IV, her blood pressure returned to 110s/50s mm Hg, but her neurologic symptoms persisted. During this period, fetal monitoring was uneventful without decelerations or bradycardia. Due to concerns for these neurologic findings, the epidural infusion was stopped, and labor allowed to progress. About 30 minutes after stopping the infusion, the patient's symptoms of facial numbness, ptosis, and miosis resolved.Within the hour, the patient desired further pain control with epidural anesthesia. Therefore, she was repositioned, and an infusion of the same solution was started at 6 mL per hour without a bolus. This was followed by an uneventful progression of labor and vaginal delivery of a healthy male infant. No further signs or symptoms of Horner's syndrome or trigeminal nerve palsy were evident during the rest of this patient's labor, de...

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