Injecting drugs into the scar: If the scar area is <15cm2, drug injection can be applied alone; if it is >15cm2, skin grafting should be performed after excision of the scar, and then drugs should be injected at the edge of the incision. Because keloid has the characteristic of infiltrating the surrounding normal skin, and the fibroblasts are the most active in the scar periphery, the injection site should be chosen at the edge of the scar first, especially for the larger scar with limited amount of drug injection at one time, in order to interrupt the infiltration of the normal skin. The method of injection is also the key to treatment. It is best to use a needleless syringe with pressure, or a small syringe with a large needle, such as a 1mL disposable syringe with a No. 7 or No. 8 needle, which is easier to inject drugs.
Clinically used drugs are as follows:
1, glucocorticoids: each point of injection 0.1mL, infiltration diameter of 0.5cm, interval 0.5 ~ 1cm, in two or three injections after the ineffective or have obvious adverse reactions should be promptly discontinued. Common complications include local tissue atrophy, necrosis, pigmentation or loss, capillary dilation, etc. Hyaluronidase: 1500 U per injection, intra-scar injection, once a month, prohibited in infected and tumor sites.
2, anti-tumor drugs: Setipec, fluorouracil ( Fu ), mitomycin, bleomycin, etc., local small dose application of adverse reactions are mild, mainly bone marrow suppression, gastrointestinal reactions, must be checked weekly blood routine. It selectively inhibits DNA, RNA and protein synthesis, thus preventing cell differentiation and replication, and its effect is 100 times stronger than that of Fu.
3, antihistamines: antihistamines inhibit the proliferation of fibroblasts and angiogenesis by inhibiting the release of histamine from mast cells.
4.Calcium channel blockers: The mechanism of scar inhibition is to block calcium channels, regulate intracellular calcium concentration, affect the synthesis of mRNA in the cell cycle, and cause skin fibroblasts to stagnate in the G1 phase. It can be used after surgical excision of the scar to perform flap grafting.
Topical agents.
Silicone gel products: Silicone gel products are non-toxic, non-irritating, non-antigenic, non-carcinogenic and non-teratogenic, safe, reliable, soft and durable. However, they cannot be used on wounds that are not completely healed, and the wounds after surgery must wait for the stitches to be removed and healed before use.
The mechanism of scar inhibition may be:
A. Decrease of water loss, increase of water content of skin stratum corneum, hydration, softening of scar;
B. Increased permeability to water-soluble proteins and various low-molecular-mass water-soluble inflammatory substances, resulting in diffusion of these proteins on the skin surface, reduction of water-soluble proteins and products in the interstitium, and reduction of fluid pressure, resulting in scar softening.
Indications:
A. Any age, any site;
B. For painful scars that restrict joint movement, which can reduce pain and allow early movement of the joint;
C. For surviving skin grafts to prevent contracture;
D. For deep II degree burn wounds, apply within 6-8 weeks after healing to prevent scar growth;
E. For advanced hypertrophic scars, to promote their softening;
F. keloid scars;
G. For medium-thick skin donor area, it can form a barrier against infection and has good water and air permeability, which can promote epithelial growth and reduce scar proliferation.
Basic fibroblast growth factor (bFGF): bFGF can stimulate fibroblasts to produce collagenase, inhibit collagen synthesis, and also promote the release of endothelial cell collagenase and fibrinogen activator, thereby inhibiting scar formation.
Capsaicin: It is possible that capsaicin has a direct inhibitory effect on some cellular components required for wound healing (e.g. Fb); secondly, it depletes the neuropeptide SP, which is mediated by the specific receptor molecule vanilloid receptor VP1 on primary afferent neuron endings and cell membranes. It also plays a regulatory role on growth factors related to wound repair, exerting a regulatory and anti-scarring effect on wound healing.
Vitamin A acid: it can inhibit intracellular DNA synthesis, thus reducing collagen synthesis; disrupt the ultrastructure of fibroblasts, such as rough endoplasmic reticulum and mitochondria, etc. Oral 25mg/d of retinoic acid for 30d; topical 0.05% retinoic acid cream for 3 months with certain effect.
Imiquimod: 5% Imiquimod cream is an immunomodulator.
Tacrolimus: Tacrolimus is a macrolide immunomodulator extracted from Streptomyces cultures. Tacrolimus can reduce the stimulatory activity of Langerhans cells isolated from human skin on T lymphocytes, and also inhibit the release of inflammatory transmitters from skin mast cells, basophils and eosinophils, with strong inhibitory effect on the release of cytokines and histamine, thus inhibiting the proliferation of fibroblasts It also inhibits the release of inflammatory transmitters from skin mast cells, basophils and eosinophils.