Acute Life-Threatening Condition Case Study Answer

Answer 1

Mrs. Casey was admitted to the emergency department with fever, suptrapubic pain, right loin flank pain, dysuria, frank haematuria and complains of myalgia and nausea. Based on nursing assessment, lab test evaluation and arterial blood gas analysis, she was suspected to suffering from urosepsis. It is a condition that leads to infection of the urinary tract and patients may present with dysuria, urinary frequency, suprapubic pain and hematuria. Patients may also show other symptoms such as fevers, flank pain, chills and nausea (Wagenlehner et al., 2017). Mrs. Casey also experienced al the above symptoms. Any form of sepsis is an interplay between host immune response, inflammatory and pro-coagulation responses. In response to invasion by any infectious agent, the toll-like receptor (TLRs) triggers an innate response of the immune cells. TLRs promotes the release of cytokine, neutrophil activation and stimulates endothelial cells. The above mechanism initiated after theyr recognize pathogen-associated molecules leading to the activation of humoral and cell-mediate immune pathways and release of pro and anti-inflammatory cytokines. In patients with severe sepsis, the release of both types of mediators significantly increases. This is followed by initiation of adaptive immunity and shift of balance towards cell death. During the last stage, programmed cell death occurs and the release and production of pro-inflammatory cytokines decreases (Mitchell & Whitehouse, 2009; Arina & Singer,2021). Thus, the above hemodynamic changes is associated with elevated cardiac output and generalized vasodilation. Increased heart rate and low blood pressure was seen for Mrs. Casey during routine nursing assessment.

There are many types of sepsis and Mrs. Casey was suspected to be suffering from urosepsis. Most of the clinical of sepsis are due to excessive inflammation. But infection triggers both pro and anti-inflammatory response lead to organ damage and secondary infection. The first phase in the pathophysiology of sepsis is the activation of innate immune cells such as macrophages, monocytes and neutrophils. The early adhesion of neutrophil and platelet is initiated by binding of the proteins by integrin. The inflammatory response is balanced by the release of anti-inflammatory mediators such as IL-4, IL-10 and epinephrine. This occurs when bacterial endotoxins binds to the receptors of the immune cells. P ro-inflammatory cytokines can also cause leukocyte activation and overexpression of endothelial adhesion molecules. This stage is followed by immunosuppressive state. This is due to apoptosis and decrease in the number of TNF and IL-6 (Guliciuc et al., 2021). However, the inflammatory system is not the only system affected in sepsis. It affects the coagulation system and the autonomic nervous system too (Wagenlehner et al., 2013).

According to Guliciuc et al. (2021), there are many cause behind coagulation disorders. In patients with severe systemic inflammation, low level of plasma C protein activates the coagulation cascade. The plasmogen tissue activators such as TNF-alpha and IL-1 beta cells are released due to expression of tissue factors in the macrophages. There is also an imbalance between fibrin formation and fibrinolysis. In case of urosepsis, it has been found that the anti-inflammatory response is generated in response to urinary tract infection. The mechanism initiates systematic inflammatory response syndrome identified 3 of the following criteria: Fever above 38 degree celcisus, tachycardia, tachypnea and leukocytosis or leukopenia. Mrs. Casey was found to be febrile and she was tachcardic as her heart rate was 124 bpm. The number of white blood cells were high evidenced by a value of 26.3x10^9/L. Thus, the activation of the immune cascade leads to a series of response in the body and the manifestation of above symptoms. The condition progresses to septic shock when the abnormalities are significant enough to increase the risk of mortality. In case of urosepsis, the cytokines has been identified as one of the major biomarker of urosepsis (Grondman et al., 2020).

Answer 2

Rationale Behind Use of Injection Ceftriaxone 1 gm IV Stat

Ceftriaxone belongs to the group of drugs called cephalosporin antibiotics. It acts by inhibiting bacterial cell-wall synthesis. The beta-lactam part of the drugs binds to endopeptidase, transpeptidases which are involved in cell wall synthesis and cell division. This binding affects the function of the enzymes thus leading to apoptosis or cell death. The study by Bery, Sodhi and Bhanot (2017) gives the evidence for the use of Ceftriaxone for the management of urosepsis. The advantage of the above mechanism of the drug is that it leads to immunosuppression and decrease in the number of cytokines such as IL-6 and TNF. So, the changes initiated can address the symptoms of Mrs. Casey and decrease the risk of adverse outcomes such as septic shock. Mrs. Casey was prescribed the medication because bacterial infection is the cause behind urosepsis and use of this drug can minimize the risk of adverse outcomes and mortality rate (Keveson & Garrison, 2017). If Ceftriaxone is not given to patient, it would lead to worsening of infection and deterioration of symptoms for patients.

Rationale Behind Use of Normal Saline 1000 ml IV Stata

Mrs. Casey has been administered normal Saline 1000 ml IV state in response to the identification of urosepsis. It is a type of crystalline fluid given to patients as part of intravenous fluid therapy. It is a crystalloid that is commonly given in shock or dehygdration to increase plasma volume. According to Semler and Rice (2016), in patients with sepsis, normal saline is given as part of fluid resuscitation. This is because patients in the early sepsis stage are frequently hypovolemic. The inflammatory process changes the vascular resistance and vascular leakage leading to decrease in stroke volume and cardiac output imbalance. Thus, the rationale behind fluid therapy is to restore cardiac output, intravascular volume and oxygen delivery. Similarly, the study by Young (2019) reports intravenous fluid therapy with crystalloids as one of the common treatment methods for management of sepsis. If normal saline is not given to patients like Mrs. Casey, there is a possibility of mortality rate and decrease in microvascular perfusion which could lead to septic shock and organ dysfunction. Thus, to avoid adverse outcomes in patients, normal saline is administered.

References

Arina, P., & Singer, M. (2021). Pathophysiology of sepsis. Current Opinion in Anesthesiology , 34 (2), 77-84.

Bery, A., Sodhi, C., & Bhanot, R. (2017). Successful management of urosepsis with ceftriaxone+ sulbactam+ EDTA: A case report of penem sparing approach. Journal of Clinical and Diagnostic Research: JCDR , 11 (9), OD18.

Grondman, I., Pirvu, A., Riza, A., Ioana, M., & Netea, M. G. (2020). Biomarkers of inflammation and the etiology of sepsis. Biochemical Society Transactions , 48 (1), 1-14.

Guliciuc, M., Maier, A. C., Maier, I. M., Kraft, A., Cucuruzac, R. R., Marinescu, M., ... & Firescu, D. (2021). The Urosepsis—A Literature Review. Medicina , 57 (9), 872.

Keveson, B., & Garrison, G. W. (2017). Urosepsis. Evidence-Based Critical Care: A Case Study Approach , 453-456.

Mitchell, E., & Whitehouse, T. (2009). The pathophysiology of sepsis. ABC of Sepsis , 20.

Semler, M. W., & Rice, T. W. (2016). Sepsis resuscitation: fluid choice and dose. Clinics in chest medicine , 37 (2), 241-250.

Wagenlehner, F. M., Lichtenstern, C., Rolfes, C., Mayer, K., Uhle, F., Weidner, W., & Weigand, M. A. (2013). Diagnosis and management for urosepsis. International Journal of Urology , 20 (10), 963-970.

Wagenlehner, F. M., Pilatz, A., Weidner, W., & Naber, K. G. (2017). Urosepsis: overview of the diagnostic and treatment challenges. Urinary Tract Infections: Molecular Pathogenesis and Clinical Management , 135-157.

Young, P. J. (2019). Balanced Crystalloids or 0.9% Saline in Sepsis. Beyond Reasonable Doubt?. American Journal of Respiratory and Critical Care Medicine , 200 (12), 1456-1458.

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