Lidocaine Toxicity Misinterpreted as a Stroke

For more than 50 years lidocaine has been used to treat ventricular arrhythmias. Neurologic dysfunction, manifested as a stroke, occurred acutely in an 87-year-old woman after she had been administered repeated doses of lidocaine, a lidocaine infusion, then an intravenous amiodarone infusion for ventricular tachycardia. This was ultimately diagnosed as lidocaine toxicity with a serum lidocaine level of 7.9 mg/L (1.5–6.0 mg/L). We discuss lidocaine toxicity and risk factors leading to its development, which include particularly hepatic dysfunction, cardiac dysfunction, advanced age and other drug administration

Lidocaine Toxicity Misinterpreted as a Stroke

For more than 50 years lidocaine has been used to treat ventricular arrhythmias. Neurologic dysfunction, manifested as a stroke, occurred acutely in an 87-year-old woman after she had been administered repeated doses of lidocaine, a lidocaine infusion, then an intravenous amiodarone infusion for ventricular tachycardia. This was ultimately diagnosed as lidocaine toxicity with a serum lidocaine level of 7.9 mg/L (1.5 - 6.0 mg/L). We discuss lidocaine toxicity and risk factors leading to its development, which include particularly hepatic dysfunction, cardiac dysfunction, advanced age and other drug administration.[West J Emerg Med. 2009;10(4):292-294.

Vascular endothelial growth factor in eye disease

Collectively, angiogenic ocular conditions represent the leading cause of irreversible vision loss in developed countries. In the U.S., for example, retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration are the principal causes of blindness in the infant, working age and elderly populations, respectively. Evidence suggests that vascular endothelial growth factor (VEGF), a 40 kDa dimeric glycoprotein, promotes angiogenesis in each of these conditions, making it a highly significant therapeutic target. However, VEGF is pleiotropic, affecting a broad spectrum of endothelial, neuronal and glial behaviors, and confounding the validity of anti-VEGF strategies, particularly under chronic disease conditions. In fact, among other functions VEGF can influence cell proliferation, cell migration, proteolysis, cell survival and vessel permeability in a wide variety of biological contexts. This article will describe the roles played by VEGF in the pathogenesis of retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. The potential disadvantages of inhibiting VEGF will be discussed, as will the rationales for targeting other VEGF-related modulators of angiogenesis