UTI - Nursing Case Study
Pathophysiology
• Primary mechanism: Bacterial ascension from the urethra to the bladder, predominantly by uropathogenic Escherichia coli, which adhere to uroepithelial cells using type 1 pili, initiating infection and inflammation.
• Secondary mechanism: Inflammatory response characterized by cytokine release (e.g., IL-6, IL-8) leading to edema and increased permeability of the uroepithelium, facilitating pathogen invasion and symptomatic manifestations such as dysuria and urgency.
• Key complication: If untreated, pathogens may ascend to the kidneys, causing acute pyelonephritis, characterized by widespread inflammation, renal tubular damage, and potential for systemic sepsis, highlighting the importance of early intervention and appropriate antimicrobial therapy.
Patient Profile
Demographics:
65-year-old female, retired nurse
History:
• Key past medical history: Chronic kidney disease stage 3, Type 2 diabetes mellitus, recurrent UTIs, hypertension
• Current medications: Metformin, Lisinopril, Furosemide, Insulin glargine, Nitrofurantoin (prophylactic)
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Severe lower abdominal pain and fever
• Key symptoms: Dysuria, hematuria, confusion, nausea, vomiting, chills
• Vital signs: Temperature 102.5°F, Heart rate 115 bpm, Blood pressure 90/50 mmHg, Respiratory rate 26 breaths per minute, Oxygen saturation 88% on room air
Section 1
Change in Patient Status:
As the clinical team continues to monitor the patient, they observe a concerning change in her status. Her mental state has deteriorated further, with increasing confusion and episodes of disorientation, suggestive of possible urosepsis. This change is accompanied by a progressive drop in blood pressure, now reading 85/45 mmHg, indicating worsening hemodynamic instability. Despite supplemental oxygen, her oxygen saturation remains suboptimal at 86%, suggesting potential respiratory compromise. The patient’s tachycardia persists, with a heart rate now at 122 bpm, and her fever remains elevated at 103°F, indicating an ongoing systemic inflammatory response.
The nursing team performs a more detailed assessment, revealing additional signs of peripheral vasoconstriction, such as cool, clammy skin and delayed capillary refill. Laboratory results reveal a significant leukocytosis with a white blood cell count of 22,000/mm³, and blood cultures are pending. Serum creatinine has risen to 2.3 mg/dL, indicating worsening renal function, likely exacerbated by the hypotensive episodes and underlying chronic kidney disease. Lactate levels are elevated at 4.2 mmol/L, further supporting the diagnosis of sepsis and highlighting the urgent need for aggressive fluid resuscitation and initiation of broad-spectrum antibiotics tailored to her penicillin allergy.
These findings necessitate immediate escalation of care. The patient is transferred to the intensive care unit for close monitoring and advanced hemodynamic support, including the initiation of a norepinephrine infusion to stabilize her blood pressure. This critical juncture in her care requires vigilant reassessment and collaboration among the interprofessional team to prevent further deterioration and optimize outcomes, particularly given her complex comorbid conditions.
Section 2
Response to Interventions:
Following the transfer to the intensive care unit, the patient is placed on continuous cardiac and hemodynamic monitoring. The team promptly initiates a norepinephrine infusion to manage her hypotension. Despite this intervention, her blood pressure remains labile, fluctuating between 80/40 mmHg and 90/50 mmHg, indicating persistent refractory hypotension. The team administers aggressive fluid resuscitation with crystalloid solutions, cautiously balancing the risk of fluid overload given her underlying chronic kidney disease.
In response to the clinical suspicion of urosepsis, the team starts broad-spectrum antibiotics, selecting a regimen safe for her penicillin allergy. After 24 hours, there is a modest improvement in her mental status; however, her confusion and disorientation persist intermittently. Her oxygen saturation shows minimal improvement, now hovering around 88% with high-flow oxygen therapy. Repeat laboratory tests reveal a slight decrease in lactate levels to 3.8 mmol/L, suggesting a partial response to the resuscitation efforts, but her renal function continues to decline, with serum creatinine rising to 2.8 mg/dL.
The patient's condition remains precarious as she develops new-onset atrial fibrillation with a rapid ventricular response, complicating her already unstable hemodynamic status. The heart rate spikes to 140 bpm, exacerbating her hypotension. The team faces a critical decision regarding the management of her arrhythmia, weighing the risks and benefits of rate control medications against the backdrop of her renal impairment and ongoing sepsis. This new complication necessitates a reassessment of her treatment plan, prioritizing interventions that will stabilize her hemodynamics while minimizing further renal insult. The interprofessional team collaborates closely to adjust her management strategy, aiming to prevent further deterioration and work towards stabilizing her condition.
Section 3
New Diagnostic Results:
As the team continues to grapple with the patient's complex condition, they decide to perform a transesophageal echocardiogram (TEE) to investigate the underlying cause of her new-onset atrial fibrillation and evaluate cardiac function in the context of her sepsis and fluctuating blood pressures. The TEE reveals moderate left ventricular systolic dysfunction with an ejection fraction of 35%, along with evidence of mild mitral regurgitation. These findings suggest that her cardiac output is compromised, likely contributing to her refractory hypotension and complicating fluid management given her chronic kidney disease.
Concurrently, the infectious disease team reviews the results of the blood cultures drawn upon admission, which now confirm the presence of extended-spectrum beta-lactamase (ESBL) producing Escherichia coli. This necessitates a shift in antibiotic strategy to include a carbapenem, carefully dosed to account for her declining renal function. Her urine culture also reveals significant growth of the same organism, reinforcing the diagnosis of urosepsis as the primary source of her systemic infection.
With these new diagnostic insights, the team is prompted to re-evaluate her treatment plan, particularly focusing on optimizing her cardiac function and targeting the resistant bacterial infection. The addition of inotropic support is considered to enhance cardiac output, while meticulous adjustment of her fluid and electrolyte balance is maintained to prevent further renal compromise. The team is acutely aware of the need for a delicate balance in the choice and dosage of medications to stabilize her, highlighting the critical importance of ongoing monitoring and clinical judgment in managing this multifaceted case.
Section 4
Change in Patient Status:
Despite the adjustments to her treatment plan, the patient's condition takes a concerning turn. Over the next 24 hours, her vital signs reveal increasing difficulty in maintaining hemodynamic stability. Her heart rate, which was initially controlled with rate-limiting agents, now fluctuates between 110 to 130 beats per minute with intermittent runs of atrial fibrillation with rapid ventricular response. Blood pressure readings become more erratic, ranging from 80/50 mmHg to 150/90 mmHg, despite the addition of inotropic support. Oxygen saturation remains stable at 94% on 2L nasal cannula, but her respiratory rate has increased to 28 breaths per minute, suggesting a compensatory response to metabolic derangements.
Laboratory results indicate a worsening metabolic acidosis with an arterial blood gas showing a pH of 7.28, bicarbonate of 16 mmol/L, and a base deficit of -8. Creatinine levels have risen to 3.2 mg/dL, indicative of acute kidney injury on top of her chronic kidney disease. Her lactic acid is elevated at 4.5 mmol/L, reflecting the ongoing tissue hypoperfusion and sepsis. Electrolyte imbalances are also noted, with potassium levels climbing to 5.8 mmol/L and sodium at 130 mmol/L, necessitating careful correction to avoid exacerbating her cardiac and renal issues.
Given these developments, the team must quickly reassess her clinical priorities. The escalating acidosis and electrolyte disturbances demand prompt intervention with cautious bicarbonate therapy and adjustments in her renal replacement therapy plan. Re-evaluation of her inotropic support and fluid management is critical to address the hemodynamic instability, while continuous cardiac monitoring remains vital to manage her arrhythmias effectively. These changes underscore the complexity of her condition, requiring advanced clinical reasoning to navigate the interplay of her cardiac, renal, and infectious processes, and foreshadow potential new complications that the team must preemptively strategize against.
Section 5
New Complications:
Despite the aggressive interventions, the patient's condition continues to deteriorate, and she develops signs of acute respiratory distress. Her respiratory rate has further increased to 34 breaths per minute, and her oxygen saturation has dropped to 88% even on a 4L nasal cannula. Auscultation of the lungs reveals bilateral crackles, suggesting pulmonary edema, possibly exacerbated by fluid shifts due to her worsening renal function and the aggressive fluid resuscitation required to maintain her blood pressure. The team performs a chest X-ray, which confirms diffuse bilateral infiltrates, consistent with acute respiratory distress syndrome (ARDS).
In parallel, the patient's neurological status declines. She becomes increasingly lethargic and difficult to arouse, with a Glasgow Coma Scale score dropping to 10. This altered mental status raises concerns about possible septic encephalopathy, worsened by the metabolic acidosis and hypoperfusion. A CT scan of the head is ordered to rule out any acute intracranial events, while an EEG is considered to assess for any subclinical seizure activity given her electrolyte imbalances.
These new complications necessitate a shift in the management plan. The decision is made to escalate respiratory support, considering non-invasive ventilation or intubation to ensure adequate oxygenation and ventilation. The fluid management strategy is revisited, aiming to strike a delicate balance between preventing further pulmonary congestion and supporting her hemodynamic stability. The team also prepares for continuous renal replacement therapy to address her worsening kidney function and electrolyte imbalances, while careful monitoring of her neurological status is imperative to guide further interventions. This complex interplay of systems failure requires the team to anticipate additional complications, such as the potential for multi-organ dysfunction syndrome, and strategize accordingly to stabilize her condition.