Effect of two-week continuous epidural administration of 2% lidocaine on mechanical allodynia induced by spinal nerve ligation in rats.

BACKGROUND: Lidocaine is an effective against certain types of neuropathic pain. This study aimed to investigate whether timing of initiating continuous epidural infusion of lidocaine affected the glial activation and development of neuropathic pain induced by L5/6 spinal nerve ligation (SNL) in rats. METHODS: Following L5/6 SNL, rats were epidurally infused 2% lidocaine (drug infusion initiated on days 1, and 7 post SNL model establishment) or saline (saline infusion initiated on day 1 post SNL model establishment) continuously for 14 days. Mechanical allodynia of the hind paw to von Frey filament stimuli was determined prior to surgery, postoperative day 3, and once weekly after SNL model establishment. At 7 days after the infusion of saline or lidocaine ended, spinal activation of proinflammatory cytokines and astrocytes was evaluated immunohistochemically, using antibodies to interleukin-6 (IL-6) and glial fibrillary acidic protein (GFAP). RESULTS: Continuous epidural administration of 2% lidocaine for 14 days increased the mechanical withdrawal threshold regardless of the difference in timing of initiating lidocaine administration. Epidurally infusing 2% lidocaine inhibited nerve ligation-induced IL-6 and GFAP activation. In the 2% lidocaine infusion group, rats maintained the increased mechanical withdrawal threshold even at 7 days after the discontinuation of 2% lidocaine infusion. CONCLUSIONS: Continuous epidural administration of 2% lidocaine inhibited the development of SNL-induced mechanical allodynia and suppressed IL-6 and GFAP activation regardless of the difference in timing of initiating lidocaine administration.

Postoperative pulmonary edema following vitrectomy in patients with ischemic heart disease and diastolic dysfunction in the post-anesthetic care unit: Two case reports.

RATIONALE: The increasing incidence of cardiac comorbidities in the elderly population has led to an increasing demand for vigilance of cardiac dysfunction induced by surgery. Favorable outcomes can be ensured in such cases by an increased awareness of cardiogenic complications, early identification of the problem, and appropriate treatment. PATIENT CONCERNS: This study presents 2 cases of acute pulmonary edema (PE) that were likely caused by ischemic heart disease and diastolic dysfunction in postoperative patients, following vitrectomy, in the post-anesthetic care unit. DIAGNOSES: Chest x-ray and computed tomography indicated PE. INTERVENTIONS: Following the diagnosis of PE, patients were intubated and transferred to the intensive care unit where 20 mg furosemide was injected and 10 µg/kg/min dobutamine was infused intravenously. OUTCOMES: On postoperative day 2, the patients' vital signs were stable and there were no signs of respiratory disturbance. LESSONS: Physicians should be alert to the potential development of PE as a postoperative complication in patients with left ventricular (LV) diastolic dysfunction and ischemic heart disease, even if the patient has undergone a procedure with mild hemodynamic change and minimal surgical stimulation such as vitrectomy. We propose that physicians treating elderly patients with LV diastolic dysfunction and ischemic heart disease undergoing vitrectomy should consider the use of intraoperative transthoracic echocardiogram or transesophageal echocardiogram with continuous monitoring of blood pressure, using devices such as arterial catheter devices.