RESUMEN
INTRODUCTION: Epidural anesthesia is commonly used for analgesia during labor, and headache is a common complaint following this procedure. Pneumocephalus, on the other hand, is a rare and potentially serious complication of epidural anesthesia, which is most often caused by accidental puncture of the dura with the introduction of air into intrathecal space. CASE PRESENTATION: We present the case of a 19-year-old Hispanic female who developed a severe frontal headache and neck pain eight hours following epidural catheter placement to deliver analgesia during labor. Physical examination was within normal limits without any neurological deficits. Computed tomography of the head and neck would later demonstrate small to moderate amounts of pneumocephalus, predominantly within the frontal horn of the lateral ventricles, and a moderate amount of air within the spinal canal. She was treated conservatively with analgesia. Though headache recurred after discharge, repeat imaging showed improvement in the volume of pneumocephalus and conservative management was continued. CONCLUSIONS: Although a rare complication and an uncommon cause of headache following epidural anesthesia, a high index of suspicion must remain for pneumocephalus as it may cause significant morbidity and, in some cases, be potentially life-threatening.
Asunto(s)
Analgesia Epidural , Trabajo de Parto , Neumocéfalo , Embarazo , Humanos , Femenino , Adulto Joven , Adulto , Analgesia Epidural/efectos adversos , Neumocéfalo/diagnóstico por imagen , Neumocéfalo/etiología , Cefalea/etiología , Manejo del Dolor/efectos adversosRESUMEN
Background: Plumbagin, a natural phenolic compound is investigated for response against blood pressure and vascular reactivity. Methodology: Blood pressure lowering effects were observed by in-vivo invasive evaluation in normotensive rats, and in-vitro experimentation to measure changes of tension in isolated rat aorta and contractility in atria. Results: The percentage decrease in mean arterial pressure (MAP) observed with plumbagin intravenously at doses of 0.1, 0.5, 1, 5, 10 âµg/kg in normotensive rats was 7.16 â± â2.35, 15.5 â± â5.62, 19.5 â± â5.27, 26 â± â6.67, 34.33 â± â8.80, respectively. Plumbagin exerted vasorelaxant effects in rat aorta, unaffected by the removal of vascular endothelium, and L-NAME and methylene blue pretreatment. Plumbagin completely inhibited phenylephrine (1 âµM) and High K+ (80 âmM) induced contractions. Similar to a Ca+2 channel antagonist, plumbagin caused a rightward shift in the Ca+2 concentration-response-curves (CRCs), resembling nifedipine. Pre-incubation with plumbagin, significantly suppressed contractions induced by phenylephrine in Ca+2-free medium via disrupting Ca+2 release from intracellular stores. No change in vasorelaxant response was observed with the addition of potassium channel blockers, TEA and BaCl2. In rat atrial strips, plumbagin exerted significant negative inotropic and chronotropic effects. No significant change was observed with atropine and atenolol pretreatment, so the effect appeared independent of muscarinic and beta-adrenergic receptors. Conclusion: This study suggests the blood pressure lowering effects of plumbagin. That could be contributed by a decrease in vascular resistance via calcium antagonism, interferences in calcium efflux, and depressive effects on the rate and force of cardiac contraction. Further studies would be necessary to probe deeper into the underlying mechanisms.