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Question 1
Mrs Smith presents with symptoms and diagnostic findings consistent with urosepsis, a systemic inflammatory response syndrome caused by an infection of the urinary tract. Mrs Smith has a urinary tract infection because her urine contains blood, nitrites, leukocytes, and a positive urine culture. Pyelonephritis can develop if the infection is not treated and spreads to the kidneys from the lower urinary tract (Hobson et al., 2018; Brown et al., 2023). The infection's bacteria may then enter the bloodstream, causing sepsis.
The raised white cell count of 26.3x10^9/L shows that Mrs Smith has a functioning disease setting off an inflammatory reaction. Since neutrophils fight bacterial infections, the high neutrophil count of 13.0x109/L indicates infection. Likewise, the high CRP level of 116 mg/L suggests infection-related inflammation. Similarly, the highly elevated procalcitonin level of 37.18 ug/L indicates a severe bacterial infection.
With a white cell count of 26.3x109/L, Mrs Smith has a disease causing her body to respond to inflammation. This reaction is reasonable for the consequence of contamination, as the high neutrophil count of 13.0x10^9/L recommends that her body is effectively fending off a bacterial disease (Hobson et al., 2018). Mrs Smith's elevated CRP level of 116 mg/L and the high neutrophil count is another vital sign of infection-related inflammation. CRP is a protein that the liver makes when there is inflammation. When there is an infection, CRP levels can rise quickly.
The diagnosis of a severe bacterial infection is further supported by the highly elevated procalcitonin level of 37.18 ug/L. Procalcitonin is a marker of bacterial infection, and when toxins from bacteria enter the bloodstream, its levels quickly rise. Therefore, the way that Mrs Smith's procalcitonin level is so high recommends that she is encountering a severe bacterial disease that requires expeditious and forceful treatment.
Mrs Smith gives fever, flank torment, sickness, and tachycardia, which are side effects generally seen with pyelonephritis and sepsis. The kidney inflammation causes flank pain, and the production of inflammatory mediators in response to infection causes the fever. A fever, sepsis, or inflammation-related side effect can cause nausea. The tachycardia is caused by the increased sympathetic activity brought on by sepsis.
With a blood pressure of 90/58 mmHg, hypotension indicates poor organ perfusion due to sepsis. Typically, hypotension raises blood pressure by activating the renin-angiotensin-aldosterone system. However, this mechanism is impaired in sepsis.
With a pH of 7.12, HCO3- levels of 16 mmol/L, and BE levels of -7.2 mmol/L, metabolic acidosis on ABGs suggests sepsis-related tissue hypoperfusion (Brown et al., 2023). The kidneys need enough blood flow to remove acids from the blood, which is reduced in sepsis, resulting in acid buildup. Because anaerobic respiration produces excessive lactate, the elevated lactate level of 5.2 mmol/L also indicates tissue hypoperfusion. It causes the acidosis seen in ABGs.
Mrs Smith is hypoxic, as evidenced by the low SpO2 of 82% and the low PaO2 of 70 mmHg. It could be because of ventilation-perfusion confusion in the lungs, a symptom of sepsis. Despite the regular respiratory rate, the low PaCO2 of 28 mmHg suggests some hyperventilation to compensate for metabolic acidosis.
She can make life changes to help her total well-being. Diet, exercise, getting enough sleep, and managing stress are essential. For example, massage therapy promotes relaxation, reduces pain, and eases muscle tension.
Mrs Smith has created urosepsis optional to pyelonephritis. Tissue hypoperfusion, organ dysfunction, and a severe acid-base disturbance have all been caused by the infection's uncontrolled systemic inflammatory response. A brief treatment of the fundamental disease, hemodynamic support, and essential consideration is expected to prevent further disintegration. By breaking the inflammatory cycle, increasing perfusion, and allowing Mrs Smith's organs to regain function, the prompt administration of these interventions, in conjunction with other supportive measures, can assist in stabilising her condition (Lehne et al., 2022; Bullock & Manias, 2022). The inability to start these medicines desperately could prompt a primary decay in Mrs Smith's state.
Question 2
Mrs Smith has been recommended ceftriaxone and intravenous liquids to treat her urosepsis. Ceftriaxone is an expansive range intravenous anti-toxin used to treat bacterial contaminations. According to FAADN, 2020, it prevents the cross-linking of peptidoglycan chains and specifically by binding to penicillin-binding proteins. It upsets cell wall arrangement, prompting cell lysis and demise. By eliminating the bacteria causing Mrs Smith's infection, ceftriaxone can help eliminate the source of her sepsis inflammation. Without antibiotic treatment, the bacteria would continue to cause inflammation and worsen organ dysfunction, acid-base imbalance, and hemodynamic instability (Fauci et al., 2022). If left untreated, this could result in multiorgan failure and septic shock.
One litre of normal saline is also crucial because it helps restore organ function, tissue perfusion, and circulatory volume, all impaired in sepsis. Normal saline infusion improves oxygen delivery throughout the body by increasing cardiac output and blood pressure (Bullock & Manias, 2022). It amends corrosive base and electrolyte irregularities, diminishes lactate levels, and forestalls irreversible organ harm. Mrs Smith's hypotension, hypoperfusion, and organ dysfunction would worsen without the regular saline infusion. Without fluid resuscitation, her acidosis and hyperlactatemia would continue to rise, resulting in irreversible organ failure (Bullock & Manias, 2022).
Mrs Smith's hypotension and organ hypoperfusion would deteriorate if the normal saline imbuement were not given. She would become increasingly unstable if she did not receive treatment, as her acid-base imbalance and lactate level would continue to rise (Bullock, S. Manias, 2022). The absence of liquid revival in sepsis can, at last, prompt irreversible organ shutdown. A significant component of any treatment plan is personal reflection. It is easier to make decisions about a patient’s health and medical care when the time is taken to comprehend their experiences, values, and priorities. It enables patients and healthcare providers to address deeper underlying issues rather than just treating superficial symptoms. Beyond just physical wellness goals, reflection also helps identify them (Penman et al., 2023; Aitken et al., 2020).
In conclusion, Mrs Smith's treatment plan relies heavily on intravenous fluid resuscitation with normal saline and ceftriaxone. Ceftriaxone disposes of the bacterial wellspring of contamination, while a typical saline mixture reestablishes dissemination, tissue perfusion, and organ capability. If these interventions were not administered promptly, Mrs Smith's condition would continue deteriorating due to uncontrolled inflammation, worsening organ dysfunction, and hemodynamic collapse. The best outcomes for patients can be achieved through a comprehensive treatment strategy incorporating conventional medicine, lifestyle modifications, and alternative treatments. However, immediate stabilisation and management of life-threatening complications are top priorities in an acute situation like sepsis.
Search engines:
CINAHL (EBSCOhost)
MEDLINE (Ovid)
Clinical Key for Nursing
Cochrane Library
JBI
Scopus
Search terms:
Urosepsis, Pyelonephritis, Sepsis, Systemic inflammatory response syndrome, Ceftriaxone, Fluid resuscitation, Normal saline, Organ dysfunction, Metabolic acidosis, Tissue hypoperfusion, Lactate, Procalcitonin, C-reactive protein, White cell count, Neutrophil, Comprehensive treatment, Lifestyle changes.
The search was conducted to locate high-quality evidence from reputable databases and sources to support the diagnosis, pathophysiology, management, and recommended lifestyle modifications discussed in the case study response.
References
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Bullock, S. Manias, E (2022). Fundamentals of pharmacundameology. 9th edn, Melbourne, VIC, Pearson Australia.
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