UTI - Nursing Case Study
Pathophysiology
• Primary mechanism: Ascending infection where uropathogens, predominantly Escherichia coli, colonize the urethra and ascend into the bladder, leading to cystitis. Bacterial virulence factors, such as adhesins, facilitate attachment to uroepithelial cells, evading urinary flow clearance.
• Secondary mechanism: Inflammatory response triggers cytokine release, causing edema and infiltration of immune cells. This inflammation can disrupt the urothelial barrier, increasing susceptibility to further bacterial invasion and potential progression to pyelonephritis.
• Key complication: Untreated progression can lead to kidney involvement with potential for acute pyelonephritis, characterized by severe systemic inflammation, renal scarring, and risk of sepsis, particularly in vulnerable populations like pregnant women and the elderly.
Patient Profile
Demographics:
65-year-old female, retired nurse
History:
• Key past medical history: Recurrent urinary tract infections, type 2 diabetes, hypertension, chronic kidney disease stage 3
• Current medications: Metformin, Lisinopril, Hydrochlorothiazide, Nitrofurantoin (prophylaxis)
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Severe lower abdominal pain and fever
• Key symptoms: Dysuria, hematuria, nausea, vomiting, confusion, chills
• Vital signs: Temperature 39.5°C (103.1°F), heart rate 120 bpm, blood pressure 85/55 mmHg, respiratory rate 24 breaths/min, oxygen saturation 90% on room air
Section 1
Initial Assessment Findings:
Upon initial assessment in the emergency department, the patient exhibits signs of systemic infection. Her mental status is notably altered; she is confused and disoriented, which is a significant change from her baseline of clear cognition. The patient's skin is clammy and pale, and her capillary refill time is prolonged at over three seconds, indicating possible hypoperfusion. Auscultation of her lungs reveals coarse crackles bilaterally, suggesting fluid overload or possible pulmonary involvement. Abdominal examination uncovers significant tenderness in the suprapubic region with positive Lloyd's sign upon percussion over the costovertebral angle, raising suspicion of pyelonephritis.
Laboratory results return quickly, revealing a white blood cell count of 18,000/µL with a left shift, indicative of an acute bacterial infection. Blood cultures are pending, but a urinalysis shows pyuria, bacteriuria, and significant hematuria. Serum creatinine is elevated at 2.6 mg/dL, a deterioration from the patient's known baseline due to her chronic kidney disease, suggesting acute kidney injury superimposed on chronic conditions. Blood glucose is markedly elevated at 320 mg/dL, consistent with her diabetes, and might be contributing to her altered mental state.
Given these findings, the clinical picture suggests a severe urinary tract infection that has likely progressed to acute pyelonephritis with systemic involvement, possibly leading to sepsis. This scenario demands immediate intervention, including aggressive fluid resuscitation, broad-spectrum intravenous antibiotics avoiding penicillin due to her allergy, and careful monitoring of her renal function. The team must also consider the possibility of diabetic ketoacidosis given her hyperglycemia and altered mental status, requiring further evaluation with an arterial blood gas and serum ketones. The next steps will focus on stabilizing her hemodynamic status and preventing further deterioration while awaiting culture results to tailor antibiotic therapy effectively.
Section 2
As the emergency department team initiates treatment, the patient receives an intravenous bolus of normal saline to address her hypoperfusion, and broad-spectrum antibiotics are administered with careful consideration of her penicillin allergy. Over the next hour, her vital signs are closely monitored. Her blood pressure initially improves from 85/50 mmHg to 95/60 mmHg, yet her heart rate remains tachycardic at 110 beats per minute. Despite the fluid resuscitation, her mental status shows minimal improvement; she continues to be confused and disoriented, prompting the need for further evaluation.
New diagnostic results return, revealing a significant metabolic acidosis with an arterial blood gas showing pH 7.28, PaCO2 32 mmHg, and HCO3- 18 mEq/L. Serum ketones are elevated, confirming the presence of diabetic ketoacidosis. Concurrently, her serum lactate level is elevated at 4.5 mmol/L, reinforcing the suspicion of sepsis. Further complicating her condition, repeat renal function tests show worsening creatinine levels at 3.0 mg/dL, indicating ongoing acute kidney injury.
In response to these findings, the clinical team adjusts the management plan to address the newly identified diabetic ketoacidosis. An insulin infusion is initiated, and electrolyte replacement is carefully managed, especially potassium, which is at the lower end of normal at 3.5 mEq/L. Continuous cardiac monitoring is implemented due to the risk of arrhythmias associated with electrolyte imbalances and her cardiac history. As her condition remains precarious, the team prepares for possible transfer to the intensive care unit for closer monitoring and advanced supportive care, highlighting the complexity and urgency of her clinical situation.
Section 3
As the clinical team closely monitors the patient, they note a subtle yet concerning change in her status. Over the next hour, despite the ongoing insulin infusion and fluid resuscitation, her confusion worsens, and she becomes increasingly lethargic. Her vital signs reveal a slight drop in blood pressure to 90/55 mmHg, while her heart rate escalates to 120 beats per minute. Her respiratory rate increases to 26 breaths per minute, indicating possible respiratory compensation for her metabolic acidosis. The team is concerned about her deteriorating mental status and the potential for further hemodynamic instability.
New laboratory results return, showing a significant drop in her potassium levels to 2.8 mEq/L, suggesting a rapid shift due to insulin therapy and ongoing acidosis. Her serum sodium has also decreased to 130 mEq/L, raising the possibility of dilutional hyponatremia from aggressive fluid administration. The team must carefully balance the need for continued fluid resuscitation with the risk of worsening electrolyte imbalances. Additionally, her renal function has deteriorated further, with creatinine now at 3.5 mg/dL, highlighting the ongoing acute kidney injury likely exacerbated by persistent sepsis and dehydration.
Faced with these complications, the clinical team quickly adjusts the management plan. They increase the frequency of electrolyte monitoring, and potassium replacement is prioritized to prevent life-threatening arrhythmias. The patient's fluid management strategy is reassessed, with isotonic saline adjustments to address the hyponatremia. Given her declining condition, the decision is made to expedite her transfer to the intensive care unit for advanced monitoring and intervention. The team prepares for potential renal replacement therapy, considering the worsening kidney function and electrolyte disturbances, underscoring the complexity and urgency of her evolving clinical picture.
Section 4
As the patient settles into the intensive care unit, her status remains precarious, and the team focuses on her response to the aggressive interventions initiated. Despite the potassium replacement and adjusted fluid strategy, the patient's condition does not stabilize as anticipated. Over the next several hours, her blood pressure continues to fluctuate, dropping to 85/50 mmHg intermittently, even with vasopressor support. Her heart rate remains persistently elevated at 125 beats per minute, and her respiratory rate now hovers around 30 breaths per minute. Her oxygen saturation begins to drop to 88% on supplemental oxygen, suggesting the development of acute respiratory distress syndrome (ARDS) in the setting of sepsis.
New diagnostic results reveal further complications. Her arterial blood gas analysis shows a worsening metabolic acidosis with a pH of 7.25 and a bicarbonate level of 16 mEq/L. Lactic acid levels have escalated to 5.5 mmol/L, indicating the severity of her systemic inflammatory response and ongoing tissue hypoperfusion. Additionally, a repeat chest X-ray displays bilateral infiltrates consistent with ARDS, compounding her respiratory compromise. The team faces the challenge of managing her complex acid-base balance and respiratory failure while preventing further renal and cardiovascular deterioration.
In light of these developments, the clinical team intensifies their efforts to stabilize the patient. They initiate non-invasive positive pressure ventilation to improve oxygenation and consider the early initiation of continuous renal replacement therapy to address her worsening renal function and electrolyte imbalances. These critical interventions are weighed carefully against the potential for further hemodynamic compromise. As the team navigates this intricate clinical scenario, they remain vigilant for any signs of multi-organ failure, fully aware that the patient's journey may demand even more intensive support in the hours to come.
Section 5
As the hours progress, the patient's condition continues to evolve, presenting new complexities that require astute clinical reasoning. Despite the initiation of non-invasive positive pressure ventilation, her oxygenation fails to improve significantly, with saturation levels persistently hovering around 86-88%. This prompts the team to escalate to invasive mechanical ventilation to ensure adequate oxygen delivery and reduce her work of breathing.
Simultaneously, the patient's renal function deteriorates rapidly. Her creatinine levels have climbed to 3.2 mg/dL, a significant rise indicating acute kidney injury likely exacerbated by ongoing hypotension and sepsis-related nephropathy. Continuous renal replacement therapy (CRRT) is commenced in an effort to manage her fluid overload, metabolic acidosis, and electrolyte disturbances, particularly hyperkalemia that has now reached 6.0 mEq/L, posing a risk for cardiac dysrhythmias.
In addition to these challenges, a new complication emerges: the patient's coagulopathy, evidenced by a prothrombin time (PT) of 22 seconds and an international normalized ratio (INR) of 2.5. The development of disseminated intravascular coagulation (DIC) is suspected, likely triggered by the severe systemic inflammatory response. This adds another layer of complexity as the team must balance the management of her clotting abnormalities with the risk of bleeding. As they adjust her treatment plan, including potential transfusions with fresh frozen plasma and platelet concentrates, the clinical team remains vigilant for signs of hemorrhage or thrombosis, aware that any misstep could tip the delicate balance they strive to maintain. These developments necessitate continuous reassessment and adjustments, keeping the team engaged in dynamic decision-making to navigate the multifaceted challenges of this critical case.