Unit 2 Assignment – Case Study 4
Carlton’s mom is concerned about the redness, heat, swelling, and pain on his foot. To provide her some reassurance, I will: (1) explain the physiologic mechanism of the inflammatory response causing Carlton’s symptoms and (2) explain how it is different from inflammation of a vital organ.
The signs and symptoms presented by Carlton are indicative of acute inflammation. According to Grossman (2014), the cardinal signs of inflammation include redness (rubor), swelling (tumor), heat (calor), pain (dolor), and loss of function (functio laesa). From the chapter cited above, we understand that redness and heat around the wound is the result of an increase in capillary blood flow due to rapid arterial and venous dilation. Also, the increase in capillary pressure and accumulation of protein-rich exudate in the tissue space (Grossman, 2014).
In comparison with the mechanism of inflammation on Carlton’s foot, the inflammation of a vital organ is more complicated. For example, a pathogen causing injury to the liver causes the release of plasma-derived inflammatory mediators into the systemic circulation (Varela, Mogildea, Moreno, & Lopes, 2018). The three-major plasma-derived mediators in plasma, namely kinins, the clotting system, and the complement cascade, exist in pre-cursor form and are activated by proteolytic enzymes (Grossman, 2014). According to Stewart and Beart (2016), kinins stimulate pain receptors and increase capillary permeability; the clotting system aims to trap foreign bodies, pathogens, and exudates; and the complement cascade promotes leukocytosis, chemotaxis, vasodilation, and phagocytosis. In return, we observe systemic manifestations of inflammation. These manifestations include fever and lethargy from the acute-phase response, elevation in erythrocyte sedimentation rate, and high-sensitivity C-reactive protein, leukocytosis, and enlargement of the lymph nodes (Grossman, 2014). These systemic manifestations enable the body to achieve optimal immune response to the pathogen. Inflammation of a vital organ, such as the liver, is mediated by plasma-derived mediators.
After interviewing Carlton and his mom, my clinical preceptor asks me to share an overview of the acute inflammatory response. In response to the request, I will discuss the immunologic events that occur in Carlton’s foot at the cellular level.
According to Grossman (2014), the two stages of the acute inflammatory response are the vascular and cellular stages, which serves to remove damaged cells, bacteria, and antigens from the site of injury. Chemical mediators are released in conjunction with the events of the vascular and cellular stages of acute inflammation. Stewart and Beart (2016) explain that mediators of the inflammatory response can either be cell (histamine and serotonin) or plasma-derived (kinins, clotting system, and complement system).
The vascular stage is defined by rapid vasodilation of the arterioles and venules, which leads to an increase in vascular permeability. Once this happens, protein-rich exudate floods out into the extravascular spaces. As the osmotic pressure increases in the interstitial space, fluid from the capillaries flow, build-up, and accumulate into the interstitial space. The build-up of fluid in the tissue space causes pain, swelling, and loss of function that is observed along with the redness and heat. To prevent the spread of infection, stagnation of blood and clotting occurs as fluid moves out of the vessels into the tissue space (Grossman, 2014).
During the cellular stage of acute inflammation, phagocytic leukocytes, such as neutrophils, migrate to the site to initiate normal functions of the immune response. The steps of leukocyte arrival at the site of injury are margination and adhesion, transmigration, chemotaxis, and phagocytosis (Grossman, 2014; Hamidzadeh, Christensen, Dalby, Chandrasekaran, & Mosser, 2017). The authors explain that during margination and adhesion, the vascular endothelium and blood leukocytes communicate with each other and leads to leukocyte accumulation along the walls of the blood vessels. Vascular endothelial cells to release cell adhesion molecules, namely selectins, allowing leukocytes to adhere to the endothelium tightly. During transmigration and chemotaxis, endothelial cells separate due to leukocyte adhesion and leukocytes to pass through the vessel wall. Chemotactic factors guide the leukocytes into the tissue spaces where they are needed. In the final stage of phagocytosis, leukocytes engulf, kill, and remove bacteria or cellular debris (Grossman, 2014).
Carlton’s mom is concerned that the wound will get worse and asks the importance of a proper diet. I will provide Carton’s mother education on the importance of vitamin A and C in proper wound healing.
Grossman (2014) explains that vitamins A and C, along with optimal levels of carbohydrates, fats, vitamins, proteins, and minerals, are critical to proper wound healing. More specifically, the author emphasizes that vitamin C is required for collagen synthesis, and vitamin A stimulates and supports epithelialization, capillary formation, and collagen synthesis. The literature suggests that without vitamin A and C, amino acid sequencing and linking does not take place, which leads to improper healing of the wound (Palmieri, Vadala, & Laurino, 2019).
Discussion
Human contamination and fecal pollution of recreational water contain diverse pathogenic bacteria posing a risk to public health. When Carlton stepped into the sharp edge of the shell, a variety of bacterial pathogens ranging from total and fecal coliforms, Escherichia coli, and enterococci were introduced into the interstitial space of his foot (Korajkic, McMinn, & Harwood, 2018). In response to the trauma, acute inflammation was triggered by cell or tissue damage and the presence of bacterial pathogens. The injury to Carlton’s foot and endotoxins produced by bacteria stimulate the release of chemokines to recruit the inflammatory response (Grossman, 2014). One of the most common mediators responsible for the inflammatory response is a cell-derived mediator called histamine. Histamine is found in high concentrations in mast cells of tissues adjacent to capillaries, blood basophils, and platelets. In response to the shell puncturing Carlton’s foot, mast cells were activated and released histamine, causing arteriole and venule to rapidly constrict and dilate (Stewart & Beart, 2016). The increased capillary permeability leads to fluid accumulation into the affected tissue, resulting in the redness, swelling, heat, pain, and loss of function that Carlton experiences.
As fluid moves out of the capillaries and into the tissue space, blood that remains in circulation thickens, flows slowly, and then clots. Phagocytic leukocytes begin to adhere and squeeze through the vessel wall and into the inflamed tissue (Hamidzadeh et al., 2017). Through chemotaxis, the leukocytes guided by chemical signals while they wander throughout the tissue (Varela et al., 2018). As they wander through the tissue, leukocytes engulf and degrade bacteria and debris through phagocytosis. The products of phagocytosis form exudates and causes Carlton further foot pain and swelling.
We understand that washing Carlton’s foot in the lake was not the best idea as it introduced more pathogens into the deep wound (Korajkic et al., 2018). Furthermore, putting on Carlton’s running shoe on the injured foot also could have introduced bacteria and fungi into the wound (Messina et al., 2015). On the other hand, Carlton’s mom was right in bringing him into the clinic for treatment. If the pathogens persist and the inflammatory response does not subside, the inflammatory response could be chronic and lead to other complications (Grossman, 2014; Varela et al., 2018).
References Cited
Grossman, S. C. (2014). Inflammation, tissue repair, and wound healing. In S. C. Grossman & C. M. Porth (Eds.), Porth’s pathophysiology: Concepts of altered health states (9th ed., pp. 306-327). Philadelphia, PA: Lipincott Williams & Wilkins.
Hamidzadeh, K., Christensen, S. M., Dalby, E., Chandrasekaran, P., & Mosser, D. M. (2017). Macrophages and the recovery from acute and chronic inflammation. Annual Review of Physiology, 79, 567-592. doi:10.1146/annurev-physiol-022516-034348
Korajkic, A., McMinn, B. R., & Harwood, V. J. (2018). Relationships between microbial indicators and pathogens in recreational water settings. International Journal of Environmental Research and Public Health, 15(12). doi:10.3390/ijerph15122842
Messina, G., Burgassi, S., Russo, C., Ceriale, E., Quercioli, C., & Meniconi, C. (2015). Is it possible to sanitize athletes’ shoes? Journal of Athletic Training, 50(2), 126-132. doi:10.4085/1062-6050-49.3.55
Palmieri, B., Vadala, M., & Laurino, C. (2019). Nutrition in wound healing: Investigation of the molecular mechanisms, a narrative review. Journal of Wound Care, 28(10), 683-693. doi:10.12968/jowc.2019.28.10.683
Stewart, A. G., & Beart, P. M. (2016). Inflammation: Maladies, models, mechanisms and molecules. British Journal of Pharmacology, 173(4), 631-634. doi:10.1111/bph.13389
Varela, M. L., Mogildea, M., Moreno, I., & Lopes, A. (2018). Acute inflammation and metabolism. Inflammation, 41(4), 1115-1127. doi:10.1007/s10753-018-0739-1
