Case Study 21
Case Study 21: Stage IV Pressure Injury (Ulcer)
The patient, 23 year-old female, came into the hospital with wound on left ischial tuberosity, weakness, 5/10 pain on numeric scale, weak hand grasps, and weak dorsi/plantar flexion bilaterally and has a history of type 1 Diabetes Mellitus (DM), smoking, and a femur fracture. Stage IV pressure injury (ulcer) will first be discussed at the cellular level. The patient’s symptom of pain will then be discussed and related to the Stage IV pressure injury. The preexisting condition of smoking will then be related to the patient’s Stage IV pressure injury.
Pressure injuries are caused by pressure on the skin and underlying structures of the skin that is not relieved for an extended amount of time (Grossman, 2014b). In this case, the patient was in long-term critical care where she was unable to be turned. A pressure injury is a form of injury that breaks down the skin and the tissues below it and can eventually lead to tissue death (Bhattacharya & Mishra, 2015). Stage IV pressure injuries include full thickness skin loss and involves damage to the muscle and bone under the skin (Bhattacharya & Mishra, 2015). Pressure from the external surface disturbs the flow of blood into the capillary bed, thus creating increased capillary pressure within the tissue (Grossman, 2014b). Grossman (2014b) says “When the pressure between a bony prominence and a support surface exceeds the normal capillary filling pressure, capillary flow essentially is obstructed” (p. 1571). The pressure causes fluid to be pushed into the interstitial space, which causes increased pressure in the vessels as well as a decreased difference in pressure between the blood in the capillary and the fluid in the tissue, creating a significantly decreased flow of oxygen to the tissues (Bhattacharya & Mishra, 2015). According to Bhattacharya and Mishra (2015), decreased circulation in the tissues makes the tissues ischemic. The lymphatic system is also unable to move through the tissues, creating a buildup of metabolic waste products in the tissues (Bhattacharya & Mishra, 2015).
If the tissues stay in this ischemic state for as little as two hours, the combination of the hypoxia and buildup of metabolic waste products will cause necrosis to take place and ulcers will start to develop (Bhattacharya & Mishra, 2015). The cell membrane of the cells begins to lose its strength and enzymes begin to break down parts of the cell due to the trauma of increased pressure (Grossman, 2014a). Once the old parts of the cell are released into circulation, cells involved in the inflammatory process, such as leukocytes and phagocytes, respond to the area where necrosis is occurring (Grossman, 2014a). When there is decreased blood flow, the inflammatory response is limited in how it is able to help, meaning necrosis is able to continue (Grossman, 2014a). According to Grossman (2014a), gangrene, which is when a large amount of tissue goes through necrosis, can occur with pressure ulcers. The dead tissue causes irritation to the other cells of the tissue and the inflammatory response is activated; however, once again, it is limited in what it can do because of the decreased flow of blood into the area (Grossman, 2014a). Since there is no inflammatory response, there is no line of demarcation between the cells of the healthy tissue and the cells of the dead tissue, so tissue death will spread rapidly amongst the cells (Grossman, 2014a).
Without the flow of blood and the retraction of lymph, erosion of the tissues occurs (Grossman, 2014c). According to Grossman (2014c), once the body detects a change in the endothelial cells in the vasculature, the inflammatory process is activated. Margination, or leukocyte accumulation, begins to happen along the endothelium wall with the help of cytokines like interleukin-1? that are released in response to stress (Grossman, 2014c). Monocytes, neutrophils, and tissue macrophages are sent to engulf bacteria and debris through opsonization (Grossman, 2014c). However, when there is decreased blood flow to the wound due to increased capillary pressure, the inflammatory response cells cannot reach the wound as quickly, if at all (Grossman, 2014c). This leads to erosion of the tissues because the body does not get the chance to fight off the increased capillary pressure (Grossman, 2014c). Bautista and Grossman (2014) say patients with pressure injuries experience pain at the site of the wound due to nociceptors that transmit the signal of the noxious stimuli, which is the decreased blood flow and retraction of lymph, into action potentials. These action potentials are sent to the dorsal horn of the spinal cord through myelinated fibers to the thalamus (Bautista & Grossman, 2014).
Nassaji, Askari, and Ghorbani (2013) state that the nicotine in cigarettes causes vasoconstriction in the capillaries at the dermal level, which leads to a decrease in blood and oxygen that is able to reach the skin tissues. Nicotine does not allow for the release of prostacyclin, which is a vasodilator that allows oxygen to reach the wound CITATION Nas13 l 1033 (Nassaji, Askari, & Ghorbani, 2013). Smoking greatly damages the endothelium lining and contributes to atherosclerosis, which blocks blood flow in the body (Conelius, 2014). This greatly increases the risk of developing a pressure injury, especially if there are other risk factors, such as the patient not being able to be turned in the ICU (Nassaji, Askari, & Ghorbani, 2013). Smoking also decreases the synthesis of collagen, which is needed to heal the wound. CITATION Nas13 l 1033 (Nassaji, Askari, & Ghorbani, 2013).
Case study 21 was admitted with a stage IV pressure injury on her left ischial tuberosity. The pressure injury was caused by a lack of mobility, leading to increased capillary pressure in the tissue and tissue necrosis. The patient complains of pain, which is related to the nociceptors signaling noxious stimuli to the brain. The comorbidity of smoking creates vasoconstriction in the vessels and atherosclerosis in the vessels, which decreases blood flow within the body. Patient was admitted recently and is currently receiving Lovenox and Lortab, has dressing changes twice a day, and is being turned in bed every two hours.
Bautista, C., & Grossman, S. (2014). Somatosensory function, pain, and headache. In S. C. Grossman, & C. M. Porth (Eds.), Porth’s pathophysiology: Concepts of altered health states (pp. 422-449). Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams ; Wilkins.
Bhattacharya, S., ; Mishra, R. (2015). Pressure ulcers: current understanding and newer modalities of treatment. Indian Journal of Plastic Surgery 48(1), 4.16. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4413488/
Conelius, J. (2014). Structure and function of the cardiovascular system. In S. C. Grossman, ; C. M. Porth (Eds.), Porth’s pathophysiology: Concepts of altered health states (pp. 712-737). Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams & Wilkins.
Grossman, S. (2014a). Cellular adaptation, injury, and death. In S. C. Grossman, & C. M. Porth (Eds.), Porth’s pathophysiology: Concepts of altered health states (pp. 101-115). Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams ; Wilkins.
Grossman, S. (2014b). Disorders of skin integrity and function. In S. C. Grossman, ; C. M. Porth (Eds.), Porth’s pathophysiology: Concepts of altered health states (pp. 1541-1581). Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams & Wilkins.
Grossman, S. (2014c). Inflammation, tissue repair, and wound healing. In S. C. Grossman, & C. M. Porth (Eds.), Porth’s pathophysiology: Concepts of altered health states (pp. 306-322). Philadelphia, PA: Wolters Kluwer Health | Lippincott Williams ; Wilkins.
Nassaji, M., Askari, Z., ; Ghorbani, R. (2013). Cigarette smoking and risk of pressure ulcer in adult intensive care unit patients. International Journal of Nursing Practice, 20(4), 418-423. Retrieved from https://doi-org.ezproxy.liberty.edu/10.1111/ijn.12141