Lidocaine and its two major metabolites may be quantified in blood, plasma, or serum to confirm the diagnosis in potential poisoning victims or to assist forensic investigation in a case of fatal overdose. Lidocaine is often given intravenously as an antiarrhythmic agent in critical cardiac-care situations. Treatment with intravenous lipid emulsions (used for parenteral feeding) to reverse the effects of local anaesthetic toxicity is becoming more common. Postarthroscopic glenohumeral chondrolysis
Lidocaine in large amounts may be toxic to cartilage and intra-articular infusions can lead to postarthroscopic glenohumeral chondrolysis. Pharmacology
Mechanism of action
Lidocaine alters signal conduction in neurons by prolonging the inactivation of the fast voltage-gated Na+ channels in the neuronal cell membrane responsible for action potential propagation. With sufficient blockage, the voltage-gated sodium channels will not open and an action potential will not be generated. Careful titration allows for a high degree of selectivity in the blockage of sensory neurons, whereas higher concentrations also affect other types of neurons. The same principle applies for this drugs actions in the heart. Blocking sodium channels in the conduction system, as well as the muscle cells of the heart, raises the depolarization threshold, making the heart less likely to initiate or conduct early action potentials that may cause an arrhythmia. Pharmacokinetics
When used as an injectable it typically begins working within four minutes and lasts for half an hour to three hours. Lidocaine is about 95% metabolized (dealkylated) in the liver mainly by CYP3A4 to the pharmacologically active metabolites monoethylglycinexylidide (MEGX) and then subsequently to the inactive glycine xylidide.
Erythema (from the Greek erythros, meaning red) is redness of the skin or mucous membranes, caused by hyperemia (increased blood flow) in superficial capillaries. It occurs with any skin injury, infection, or inflammation. Examples of erythema not associated with pathology include nervous blushes. Types
Erythema ab igne
Erythema chronicum migrans
Erythema induratum
Erythema infectiosum (or fifth disease)
Erythema marginatum
Erythema migrans
Erythema multiforme (EM)
Erythema nodosum
Erythema toxicum
Erythema elevatum diutinum
Erythema gyratum repens
Keratolytic winter erythema
Palmar erythema

Causes
It can be caused by infection, massage, electrical treatment, acne medication, allergies, exercise, solar radiation (sunburn), photosensitization, acute radiation syndrome, mercury toxicity, blister agents, niacin administration, or waxing and tweezing of the hairs—any of which can cause the capillaries to dilate, resulting in redness. Erythema is a common side effect of radiotherapy treatment due to patient exposure to ionizing radiation. Diagnosis
Erythema disappears on finger pressure (blanching), while purpura or bleeding in the skin and pigmentation do not. There is no temperature elevation, unless it is associated with the dilation of arteries in the deeper layer of the skin. See also
Hyperemia
Flushing (physiology)
List of cutaneous conditions

References


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