Answer To: 15 refrences please
Dr. Saloni answered on May 19 2024
14
Case Study
Patient Assessment
Shaun have been suffering from major respiratory distress as well as systemic indications of infection, indicating sepsis following pneumonia (Bruse et al., 2022). Patients who have sepsis initially in the presentation period typically exhibit the following change in vital signs:
· A fever, or a temperature more than 38 C
· Increased Heart Rate (Tachycardia): HR 124 bpm
· A High Respiratory Rate, also known as Tachypnea: RR 30 bpm
· A Low Blood Pressure (Shaun has Hypotension): BP 95/56 mmHg
· Inadequate Perfusion as well as Hypoxia: Shaun also has Pallor, cold, clammy skin, and a SpO2 of 91% on room air.
· Nutritional Inadequacies: Shaun may have loss of weight and appetite, which led him to be weak.
· Dehydration and Renal dysfunction: Shaun also has cracked tongue, dryness of lips, and reduced urine production since 9 am (Marques et al., 2023).
Comprehensive Nursing Assessment
In the case of Shaun, nurse should thoroughly assess end-organ function and peripheral perfusion to ascertain their area in the pathophysiologic progress of sepsis. The assessment should include:
· Urine output analysis
· Mixed venous saturation evaluation
· Glasgow Coma Scale (GCS)
· Psychological assessment.
Urinalysis, source cultures (blood, urine), and a complete blood count should also be assessed in case of Shaun including differential (CBC-d) (Shappell et al., 2023). Additional laboratory investigations can also reveal crucial information on the sepsis severity in Shaun, which include an arterial blood gas, a disseminated intravascular coagulation screen, chemistry profile, and liver function tests. It is advised to perform at least 2 rounds of blood cultures before giving antibiotics. An x-ray of the chest may show evidence of ARDS or pneumonia. If Shaun develops necrotizing fasciitis, simple X-rays of the limbs could show gas in the tissues. The gallbladder can be evaluated with ultrasound. To check for ischemia, intestinal perforation, or abscess in the belly, a CT scan is performed (Unterberg et al., 2022).
Disease Pathophysiology and Complications
A potentially fatal medical emergency, sepsis is often referred to as blood poisoning or septicemia. It develops when the body's immune system responds inappropriately to an infection, causing injury to its own cells and tissues. The extensive pathophysiology of sepsis is triggered by the consequences of persistent bacteremia-induced circulating bacterial products, which are regulated by cytokine release. The host's clinically noticeable symptoms of bacteremia are caused by cytokines. The initial signal is the identification of endogenous host-generated danger signals and molecular patterns caused by pathogens (Schiavello et al., 2023).
In Shaun’s case, he has been suffering from hypotension; the patient is now classified as having severe sepsis when tissue oxygenation is unable to sufficiently meet tissue demands due to the onset of hypotension. Cellular and metabolic abnormalities result from a decrease in peripheral vascular perfusion as well as oxygenation. Most prominently, this causes a change in respiration from aerobic to anaerobic, which causes lactic acidosis (Herminghaus & Osuchowski, 2022).
Identification of endogenous host-derived danger signals or pathogen-derived molecular patterns serves as the initial signal. Through the genes transcription that regulate inflammation, adaptive immunity, and cell metabolism these chemicals activate specific receptors on the outer layers of antigen-presenting cells and monocytes, consequently initiating the clinical syndrome underlying sepsis. Despite the upregulation of both pro- and anti-inflammatory channels, the inflammation that results eventually causes multi-organ dysfunction by producing progressive damage to tissues. Concomitant immunosuppression, resulting from diminished activating cell surface molecules, elevated immune cell apoptosis, and T cell exhaustion, causes "immunoparalysis" in the the later phases of the condition's course and leaves affected patients vulnerable to opportunistic pathogens, viral reactivation, and nosocomial infections in many patients (Ahlström et al., 2022). As a consequence of signal transduction driven by DAMPs and PAMPs binding to TLRs on monocytes and APCs, nuclear factor-kappa-light-chain activator of activated B cells is translocated into the cell nuclei. Interferons, tumor necrosis factor alpha, pro-inflammatory interleukins such as IL-12, IL-1, IL-18, and others are among the "early activated genes" that are expressed as a result. These then trigger the activation of other cytokines (including IFN-y, IL-8, and IL-6), complement, including coagulation pathways. Additionally, through negative feedback, they cause a diminution of adaptive immune system molecules (Nishibori, 2022). Raised levels of cytokines that are both pro- and anti-inflammatory are indicative of these mechanisms in the initial phases of septic illness. Overall, the immunological phenotype (hyper- vs. hypo-responsiveness) is still very individualized, which makes diagnosis extremely challenging (Batra et al., 2022). Neutrophils are an important component of the body's initial stage of protection against pathogens since they are a part of the immune system that is innate. Through acute granulocyte maturation, significant bacterial infections cause the bone marrow to discharge both immature and mature neutrophil types. Immature neutrophils exhibit decreased phagocytosis along with oxidative burst capacity while stimulated by DAMPs or PAMPs (Baghela et al., 2023).
Additionally, Shaun is at risk of developing septic shock. Septic shock develops when sepsis-induced hypotension is not responsive to early fluid resuscitation therapy. Being a distributive kind of shock, septic shock differs from other types of shock states. Histamine, super-radicals, lysosomal enzymes, and serotonin are among the inflammatory mediators that are produced in reaction to bacterial endotoxins. These mediators cause a significant decrease in peripheral vascular resistance and a rise in capillary permeability. This results in a decrease in venous...