Pharmacology
Chlordiazepoxide acts on benzodiazepine allosteric sites that are part of the  GABAA receptor/ion-channel complex and this results in an increased binding of the inhibitory neurotransmitter GABA to the GABAA receptor thereby producing inhibitory effects on the central nervous system and body similar to the effects of other benzodiazepines. Chlordiazepoxide is anticonvulsant. There is preferential storage of chlordiazepoxide in some organs including the heart of the neonate. Absorption by any administered route and the risk of accumulation is significantly increased in the neonate. The withdrawal of chlordiazepoxide during pregnancy and breast feeding is recommended, as chlordiazepoxide rapidly crosses the placenta and also is excreted in breast milk. Chlordiazepoxide also decreases prolactin release in rats. Benzodiazepines act via micromolar benzodiazepine binding sites as Ca2+ channel blockers and significantly inhibit depolarization-sensitive Calcium uptake in animal nerve terminal preparations. Chlordiazepoxide inhibits acetylcholine release in mouse hippocampal synaptosomes in vivo. This has been found by measuring sodium-dependent high affinity choline uptake in vitro after pretreatment of the mice in vivo with chlordiazepoxide. This may play a role in chlordiazepoxides anticonvulsant properties. Pharmacokinetics
Chlordiazepoxide is a long-acting benzodiazepine drug. The half-life of Chlordiazepoxide is 5 – 30 hours but has an active benzodiazepine metabolite (desmethyldiazepam), which has a half-life of 36 – 200 hours. The half-life of chlordiazepoxide increases significantly in the elderly, which may result in prolonged action as well as accumulation of the drug during repeated administration.
Stasis dermatitis refers to the skin changes that occur in the leg as a result of "stasis" or blood pooling from insufficient venous return; the alternative name of varicose eczema comes from a common cause of this being varicose veins.Insufficient venous return results in increased pressure in the capillaries with the result that both fluid and cells may "leak" out of the capillaries. This results in red cells breaking down, with iron containing hemosiderin possibly contributing to the pathology of this entity. Symptoms
Stasis dermatitis may be characterized by:

Skin that appears thin, brown and tissue-like, with possible skin lesions (macule or patches), red spots, superficial skin irritation and/or darkening and/or thickening of the skin at the ankles or legs
Weak skin may ulcerate in some areas and legs, ankles, or other areas may become swollen
Open sores, ulcers
Itching and/or leg pains
Sometimes pain may persist from swollen tissues and may feel like "stabbing" or "needle pricks"If skin continues to deteriorate and breaks down, a venous ulcer (also known as a stasis ulcer) may form. Without proper wound care, open cracks predispose patients for the entry of a bacterial infection, causing cellulitis in the leg. Diagnosis
Stasis dermatitis is diagnosed clinically by assessing the appearance of red plaques on the lower legs and the inner side of the ankle. Stasis dermatitis can resemble a number of other conditions, such as cellulitis and contact dermatitis, and at times needs the use of a duplex ultrasound to confirm the diagnosis or if clinical diagnosis alone is not sufficient.