Cutaneous Necrosis

The incidence of cutaneous necrosis does not discriminate between sclerosing agents.Necrosis can result from extravasation of a sclerosing solution into the perivascular tissue, injection into a dermal arteriole or an arteriole feeding into a telangiectatic or varicose vein, a reactive vasospasm of the vessel, injection of a sclerosant in higher concentrations than required for the treatment vessel diameter or excessive cutaneous pressure created by compression techniques [2, 3, 24]. Due to the degree of possible human error, the injection technique is an important, but not foolproof, factor in avoiding this complication, even under optimal circumstances. Polidocanol appears to be the least toxic sclerosant to subcutaneous tissue (Tables 8.8 and 8.11).However, in sufficient concentrations, it has been reported to cause cutaneous necrosis (concentrations greater than 1%) [2, 25, 26]. Excessive compression of the skin overlying the treated vein may produce tissue anoxia with the development of localized cutaneous ulceration and may ultimately produce tissue ischemia. Therefore, it is recommended that patients not wear a graduated compression stocking of over 30–40 mmHg for long periods of time when the patient is recumbent [2].Whatever the cause of the ulceration, institution of treatment at the time of occurrence is optimum. Fortunately, most ulcers that occur are small (24-mm diameter), and primary healing usually leaves an acceptable scar. For larger ulcers, hydrocolloid or saline wet-to-dry dressings result in a decreased healing time after proper wound debridement. Excision and closure of these lesions is also recommended, as this affords the patient the fastest healing and an acceptable scar.

Table 8.8. Sclerosing agents   Classes   Agents   FDA approval   Ingredients   Advantages   Disadvantages   Osmotic agents   Hypertonic saline   Approved abortifacient   18–30% saline   Lack of allergenicity   Damage to cellular tissues Produce ulcerations Necrosis Hyperpigmentation Pain Muscle cramping       Hypertonic glucose/saline (Sclerodex)   Not approved   250 mg/ml of dextrose, 100 mg/ml of sodium chloride, 100 mg/ml of propylene glycol, and 8 mg/ml of phenethyl alcohol   Minimized pain Less muscle cramping   Superficial necrosis Allergic reaction Hyperpigmentation Mild pain   Chemical irritants   Chromated glycerin (Scleremo)   Not approved   1.11% chromated glycerin   Rare posttreatment hyperpigmentation, necrosis, and bruising, even if injected extravascularly   Weak agent, therefore requires more treatment sessions High viscosity Pain       Polyiodinated iodine (Variglobin, Sclerodine)   Not approved   A water solution of iodide ions, sodium iodine, and benzyl alcohol   Direct destruction of the endothelium   Necrosis Pain   Detergent sclerosing solutions   Sodium morrhuate   Approved   Sodium salts of the saturated and unsaturated fatty acids in cod-liver oil   N/A   Extremely caustic Necrosis Allergic reactions, including anaphylaxis Pain       Ethanolamine oleate (Ethamolin)   Not approved   Ethanol amine and oleic acid   Decreased risk of allergic reaction   Hemolysisa Renal failure with recoverya Constitutional symptomsa Pulmonary toxicity Allergic reactions Pain       Sodium tetradecyl sulfate   Approved   Sodium 1-isobutyl-4-ethyloctyl sulfate, benzoyl alcohol 2% (anesthetic), and phosphate   N/A   Epidermal necrosis Allergic reaction Hyperpigmen-tationb Pain       Polidocanol (Aethoxysklerol)   Pending   Hydroxypolyeth- oxydodecane, distilled water, and ethyl alcohol   Will not produce ulcerations Necrosis is very rare Allergic reaction is very rare Less hyperpigmentation Painless   Necrosis (rare)a Allergic reaction (rare)     a Dose related b Posttreatment hyperpigmentation is worse than with that of all other sclerosing solutions

Table 8.11. Complications and risks of sclerotherapy Allergic reaction, including anaphylaxis Hyperpigmentation Necrosis Nerve damage Orthostatic hypotension Scintillating scotomas Telangiectatic matting Thromboembolism Thrombosis (deep or superficial) pulmonary embolism Thrombophlebitis