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Introduction
The inflammatory process is a mechanism in which the body defends itself from any injury while hyperemia is the instant presence of an abnormally large blood supply from a dilated blood vessel with slow blood flow (Netpub.com, 2011). This vessel later becomes more permeable allowing macro and micro molecules vital for the wound healing process and protection against infectious materials to be localized in the affected area. Exudation will follow as a result of fluid accumulation on the injured area also resulting in edema; this is then followed by the healing process (Chris, 2006).
Wound healing is a complex body process involving cell organization and extracellular matrix formation required to repair the damaged tissue; immediately after tissues damage, the repair process comprising of active molecular meant to restore the worn-out cells and tissues begins following the inflammatory phase (Netpub.com, 2011). The prostaglandins which are chemical mediators produced by inflammatory cells increase the permeability of blood micro-vessels thereby allowing migration of blood cells to the affected area (Mendonça and Coutinho, 2009). The activated macrophage which is the main effectors cell secretes chemotactic factors and growth factors (TGF-ALPHA, PDGF, and fibroblast growth mediators), which are the main cytokines used for the formation of granulation tissues (Mendonça and Coutinho, 2009).
The proliferative phase is the second step which primarily involves the closing of the lesion; a few hours after lesion formation, re-epithelialization starts; where epithelial and epidermal cells coming from the lesion margins take over the damaged tissue (Mendonça and Coutinho, 2009). The fibroblasts present produces a new extracellular matrix responsible for cell growth and formation of new blood vessels, this is later followed by vascular permeability, where the newly formed blood vessel increases its permeability to water and other important macromolecules resulting in edema formation (Mendonça and Coutinho, 2009).
In the angiogenesis phase, new blood vessels formed from preexisting ones are used in the formation of temporal granular tissue, which aids in supplying nutrients and oxygen to the growing tissues (Mendonça and Coutinho, 2009). The extracellular matrix formation step involves the development of new capillaries and the migration of epithelial cells. This is followed by the production and organization of important extracellular matrix such as collagen, fibronectin, vitronectin, tenascin, and pigments laminin (Mendonça and Coutinho, 2009); all this play a vital role in the maintenance of blood vessels and cellular growth.
The remodeling phase is then followed by active healing and recovering of the normal tissue structures and the extracellular matrix matures initiating the deposition of collagen and proteoglycan materials forming a transient matrix (Mendonça and Coutinho, 2009). This is accompanied by apoptosis, phenotypically perceived as scar or keloids; when the wound is completely healed the scar peels off (Mendonça and Coutinho, 2009).
Major signs and symptoms of an inflammatory response
There are four popular major signs and symptoms of all categories of inflammation (Chris, 2006); once an injury has occurred to the body of an organism, for instance, the minute blood vessels called arterial in the surrounding affected tissue dilate. This dilation will then increase blood flow to the injured area resulting in a visible redness (reddening) of the area, this is followed by an increase in blood vessels permeability caused by vasoactive substances which increases the pore size of the arterials localizing blood cells, chemicals mediators, blood proteins and fluids to the affected area which therefore results to swelling (Chris, 2006). As a result of this swelling, the nerves fibers in the area are squeezed and compressed causing pain to the organism (Chris, 2006). Irritation of the nerves may also follow contributing further to the painful experience caused by prostaglandins which are inflammatory chemical mediators produced in the process (Chris, 2006).
The blood will actively transport to the affected area individual blood components to carry out their respective functions, for example, the white blood cells (leucocytes) will play a vital role in engulfing and attacking all types of invading microorganisms. Platelets (thrombocytes) will have a role in blood clotting and stop blood loss in case of any bleeding; all these active chemical processes taking place during inflammation will be followed by heat production alongside increased blood flow to the affected area (Chris, 2006). Moreover, the affected inflamed area will lose its function and becomes dormant until the healing process is over; note that not all signs and symptoms of inflammation are evident (Chris, 2006).
Recommendations on diagnostic/laboratory procedures to assess the presence and severity of inflammation and cellular injury
Diagnostic blood tests to detect and determine the level of inflammation include erythrocyte sedimentation rate (ESR) and C-reactive protein (Patient.com, 2010). These tests are very useful for not only diagnosing inflammation but also for monitoring activities of certain diseases that might be present. Erythrocyte sedimentation rate blood test involves; first, a blood sample is removed from the patient and placed on a clean sterile graduated tube in millimeters which contain an anti-clotting factor that would prevent it from coagulating or clumping (Patient.com, 2010). The tube is then left to stand while upright and after a few minutes, the red blood cells (erythrocytes) and other cells will separate and settle at the bottom of the tube as sediments leaving a clear liquid called plasma at the top (Patient.com, 2010).
This sedimentation rate is normally measured in millimeters per hour (mm/hr); the principles behind this sedimentation rate is that if there are any proteins produced by the body as a defense mechanism against inflammation, the proteins will stick on to the red blood cell, will become heavier than normal erythrocyte weight and sediments more quickly (Patient.com, 2010). Therefore, diagnostic interpretation is that the faster the sedimentation rate indicates the presence of some inflammations in the body (Patient.com, 2010).
C-reactive protein (CRP) is sometimes referred to in medical terms as acute-phase protein; this means that when you have some diseases that may cause inflammation conditions, the levels of C-reactive proteins in the body rise. These levels are promptly measured using the patients blood samples; CPR is noted to be a marker of inflammation and other abnormalities when its levels increase in the blood. Normal body CRP concentration is below 10 mg/L but slightly increases with age (Patient.com, 2010). The results are interpreted after 25 minutes of the diagnosis.
Many analytical tests can be used to determine CPR levels including Enzyme-linked immunosorbent assay, immunoturbidimetry, rapid immunodiffusion, and visual agglutination among others (Patient.com, 2010). However, changes in CPR levels occur rapidly and can be within the first days of treatments which is a clear indication that the patient is responding to treatment well (Patient.com, 2010). If the CPR levels dont drop down with continued treatment, it may indicate that the treatment is not working, and this may force the physician to switch to other treatments options. Both tests; CPR and ESR are very useful non-specific tests that only alert that there are some abnormalities, but more advanced tests will be required for clarifying the specific cause of the illness (Patient.com, 2010)
Source: (Medinet.com, 2011); (Hamilton, 2005).
References
Chris, L. (2006). Inflammation Causes, Symptoms, Process, Treatment. Web.
Hamilton, S. (2005). Managing Blood Tests and Blood Abnormalities. Web.
Mendonça, R. & Coutinho, J. (2009). The Wound Healing Process: Inflammatory, Proliferative and Remodeling Phases. Web.
Medinet.com, (2011). Body electrolytes. Web.
Netpub.com, (2011). Inflammation process. Web.
Patient.com, (2010). Blood tests detecting inflammation. Web.
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