The skin after micropigmentation
Acute skin inflammation following micropigmentation
Acute inflammation is a short-term process, usually appearing within a few minutes of the cell trauma being induced by micropigmentation. Damage occurs from the initial trauma to the cells and tissues, where the local network of ruptured blood vessels bleed into the tissue spaces and the cell walls rupture. Cellular damage occurs, leaving dead and dying cells disrupted by the trauma. Within seconds and up to 10 minutes after the initial trauma, local blood vessel constriction occurs. This vasoconstriction minimises blood loss from the area and initiates clotting (haematoma), and causes stimulation of the surrounding pain receptors. However, the resulting hypoxia causes tissue necrosis at the primary injury site. This triggers the lysosomes (waste disposal unit within a cell) found within the dead and damaged cells to start to leak digestive enzymes through their ruptured membranes. These enzymes act as inflammatory mediators causing surrounding arterioles and capillaries to dilate; pain receptors are specialised nerve endings located throughout the body in most body tissues.
Once the nerve endings are stimulated by these chemicals, they begin firing the nerves that are connected to them and send pain signals to the spinal cord and brain. As blood vessels dilate, they become more permeable and within a few hours, exudation increases.
As the vessel walls enlarge, the speed of flow decreases due to vessels being packed with cells. The stasis of blood allows leukocytes to move along the endothelium and escape through the capillary wall, along with plasma and other circulating defensive substances such as antibodies, phagocytes, and fibrinogen to the site of the injury.
The arrival of these specialised cells (antibodies, phagocytes) lead to the engulfing of dead cells, foreign material or infectious agents. As fluid moves out of the capillaries, stagnation of flow and clotting of blood in the small capillaries occurs at the site of injury. This process is caused as fibrinogen produces fibrin which forms a mesh of fibres creating a collection site for red blood cells (haematoma) and also traps micro-organisms preventing their movement further from the injury site.
This increased collection of fluid into the tissue spaces causes it to swell (tumour). This expansion of chemical activity in surrounding tissues produces the zone of secondary injury. Normally, lymphatic vessels drain the area of excess fluid and cells. However, following trauma within the tissues, the lymph vessels become blocked. The excess fluid and cells collect in the spaces between the tissues around the site of the trauma, and oedema occurs. As fluid and cells try to occupy a limited amount of space, the pressure caused by nerve endings is perceived as pain.
A large number of lymphatic channels lie directly beneath the skin. Oedema, which is the swelling or natural splinting process of the body, has two basic components. The first is a liquid, which can be evacuated by the circulatory system and the second is comprised of proteins that have to be evacuated by the lymphatic system.
The lymph vessel diameter and the flow of the lymph system being decreased cause the swelling to occur in the first 24 hours following micropigmentation. Within 12 hours of injury, macrophages move into digest tissue debris to clear the way for peripheral cells to begin the process of mitosis. Fibrocytes also move into the area to start the process of fibroplasia. Tissue repair overlaps the inflammatory process, and within 48 to 72 hours, the haematoma is sufficiently diminished to allow for this new growth of tissue. As the damaged skin within the epidermal layers begins to regenerate, the deeper soft tissues will replace damaged cells with scar tissue. The fibroblasts release collagen, elastin and reticulin fibres, forming a mesh network to reconnect tissues.
Over the next three day’s mitosis continues, and all around the injured area, capillary loops develop (angiogenesis). These sprouting vessels originate from pre-existing vessels and appear as minute red granules, hence the name granulation tissue. As the circulation is increased by these additional blood vessels replacing damaged ones, more oxygen and nutrients become readily available to these cells to aid in speeding up the healing process. When circulation is increased, it automatically increases lymphatic flow with the movement of tissue fluid between the two systems, allowing the excess buildup of lymph to be drained, reducing swelling.
Inflammation is the important first stage of healing damaged tissue. Healing cannot occur until inflammation has come and gone. Therefore we cannot prevent inflammation; however, we can speed up the processes involved by application of cold therapies following micropigmentation for the first 72 hours following treatment.
Whenever trauma occurs to the surface of the epidermis, the protective barrier will be impaired; the application of micropigmentation treatment will cause a burn, cut or puncture wound to the area infused with pigment. The epidermis will protect this impairment by the formation of a scab; the size and extent of this scab will be in relation to the trauma caused. The scab may be minute and clearer in colour if only lymph vessels have been disturbed; however, if capillary damage was involved, there would be droplets of blood also in the scab formation.
When treating more mature clients or clients with more sensitive skin, there is a higher tendency to bruise and tear the skin resulting in a greater inflammatory response. This will result in a slightly longer healing process. The healing process can differ from one client to another; there are several factors to consider, such as:
- Age
- Health of client
- Client lifestyle; as a rule, the older you are (once passed 25 years), the slower the expected healing rate. Remember, the superficial tissues will display signs of healed skin long before the internal layers have completed the full healing process.