Livedoid dermatitis is a iatrogenic cutaneous reaction that occurs immediately after a drug injection. It presents as an immediate, extreme pain around the injection site, with overlying skin rapidly becoming erythematous, violaceous, or blanched ("ischemic pallor"): 124  and sometimes with reticular pattern. The reaction eventually leads to variable degrees of necrosis to the skin and underlying tissue. The wound eventually heals, but can lead to atrophic, disfiguring scarring. The reaction is associated with a range of both injection sites and drugs. It was first reported by Freudenthal in 1924 following an injection of bismuth salts for syphilis. Although initial reports were following intramuscular injections, the reaction has since also been reported following subcutaneous, intravenous, and intraarticular injections. Livedoid dermatitis has been reported to occur with many different drug injections, including: penicillins, local anesthetics (e.g. lidocaine), vaccines (e.g. Dtap), corticosteroids, NSAIDs, and more. Presentation
Pathogenesis
The cause of this condition is poorly understood. Microscopic examination of affected tissue shows ischemic necrosis, and so various hypotheses exist to explain this ischemia, including vasospasm from needle prick, the injected drug, or cold compresses applied to the wound. Diagnosis
The diagnosis is mainly clinical. Skin biopsies of the site show necrosis caused by ischemia. Radiographic imaging may help to delineate the extent of the wound. Treatment
Depending on the extent and state of infection of the wound, the condition may require antibiotics, wound debridement in early stages, and corrective plastic surgery in late stages. See also
Injection site reactions
List of cutaneous conditions


== References ==
Primary Raynauds is thought to be at least partly hereditary, although specific genes have not yet been identified.Smoking increases frequency and intensity of attacks, and a hormonal component exists. Caffeine, estrogen, and nonselective beta-blockers are often listed as aggravating factors, but evidence that they should be avoided is not solid. Secondary
Raynauds phenomenon, or secondary Raynauds, occurs secondary to a wide variety of other conditions. Secondary Raynauds has a number of associations:
Connective tissue disorders:
Scleroderma
Systemic lupus erythematosus
Rheumatoid arthritis
Sjögrens syndrome
Dermatomyositis
Polymyositis
Mixed connective tissue disease
Cold agglutinin disease
Ehlers-Danlos syndrome
Eating disorders:
Anorexia nervosa
Obstructive disorders:
Atherosclerosis
Buergers disease
Takayasus arteritis
Subclavian aneurysms
Thoracic outlet syndrome
Drugs:
Beta-blockers
Cytotoxic drugs – particularly chemotherapeutics and most especially bleomycin
Cyclosporin
Bromocriptine
Ergotamine
Sulfasalazine
Anthrax vaccines whose primary ingredient is the Anthrax Protective Antigen
Stimulant medications, such as those used to treat ADHD (amphetamine and methylphenidate)
OTC pseudoephedrine medications (Chlor-Trimeton, Sudafed, others)
Occupation:
Jobs involving vibration, particularly drilling and prolonged use of a string trimmer (weed whacker), experience vibration white finger
Exposure to vinyl chloride, mercury
Exposure to the cold (e.g., by working as a frozen food packer)
Others:
Physical trauma to the extremities
Lyme disease
Hypothyroidism
Cryoglobulinemia
Cancer
Chronic fatigue syndrome
Reflex sympathetic dystrophy
Carpal tunnel syndrome
Magnesium deficiency
Multiple sclerosis
Erythromelalgia (clinically presenting as the opposite of Raynauds, with hot and warm extremities, often co-exists in patients with Raynauds)
Chilblains (also clinically presenting as the opposite of Raynauds, with hot and itchy extremities, however it affects smaller areas than erythromelalgia, for instance the tip of a toe rather than the whole foot)Raynauds can precede these other diseases by many years, making it the first presenting symptom.