uti - Nursing Case Study
Pathophysiology
• Primary mechanism: Bacterial invasion - Most UTIs are caused by Escherichia coli, which ascend from the urethra into the bladder. These bacteria adhere to the uroepithelial cells using fimbriae, leading to colonization and infection.
• Secondary mechanism: Host response - The presence of bacteria triggers an immune response, resulting in inflammation. The release of cytokines and chemokines attracts white blood cells to the site, causing symptoms like dysuria and frequency.
• Key complication: If untreated, the infection can ascend to the kidneys, leading to pyelonephritis. This condition is marked by fever, flank pain, and can result in renal scarring or sepsis, emphasizing the importance of early diagnosis and treatment.
Patient Profile
Demographics:
32-year-old female, office administrator
History:
• Key past medical history: Recurrent urinary tract infections, hypertension
• Current medications: Lisinopril 10 mg daily, Nitrofurantoin 100 mg twice daily
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Severe lower abdominal pain and increased urinary frequency
• Key symptoms: Dysuria, hematuria, fever, chills, back pain
• Vital signs: Temperature 101.4°F, heart rate 105 bpm, blood pressure 150/95 mmHg, respiratory rate 22 breaths per minute
Section 1
The initial assessment findings reveal notable concerns that necessitate further investigation and intervention. The patient's vital signs indicate a febrile state with a temperature of 101.4°F, tachycardia with a heart rate of 105 bpm, and elevated blood pressure at 150/95 mmHg. Her respiratory rate is slightly elevated at 22 breaths per minute, suggesting mild respiratory distress possibly due to pain or fever. Upon physical examination, there is tenderness in the suprapubic region and significant costovertebral angle tenderness on palpation, suggesting potential kidney involvement. The patient's urine appears cloudy with a strong odor, and dipstick analysis shows positive leukocyte esterase and nitrites, indicative of a bacterial infection.
Laboratory results further corroborate the suspicion of a worsening urinary tract infection with potential progression to pyelonephritis. The complete blood count reveals leukocytosis with a white blood cell count of 15,000/mm³, suggesting an active systemic inflammatory response. Serum creatinine levels are slightly elevated at 1.4 mg/dL, indicating possible renal involvement. Blood cultures are pending, but preliminary urinalysis cultures show heavy growth of Escherichia coli, consistent with the patient's history of recurrent UTIs.
Given these findings, the immediate clinical reasoning involves determining the appropriate escalation of care. The presence of flank pain, fever, and hematuria, combined with the elevated creatinine, suggests that the infection may have ascended to the kidneys, necessitating initiation of intravenous antibiotics to prevent further complications such as renal scarring or sepsis. The patient's history of hypertension also requires close monitoring of blood pressure, as it may be exacerbated by the infection or treatment. These developments guide the need for hospitalization and a multidisciplinary approach to management, focusing on aggressive antibiotic therapy and supportive care to stabilize her condition.
Section 2
As the patient is admitted to the hospital, the medical team initiates intravenous antibiotic therapy with ceftriaxone to target the suspected E. coli infection. Within the first 24 hours, the patient's clinical status is closely monitored. Despite the aggressive antibiotic treatment, there is a concerning change in her condition. Her fever persists, with a temperature now reaching 102.2°F, and her heart rate remains elevated at 110 bpm. Her blood pressure fluctuates, occasionally dropping to 130/80 mmHg, which may indicate the early onset of systemic involvement. Additionally, the patient reports increased flank pain and a new onset of nausea and vomiting, raising suspicion of further complications.
New diagnostic tests are ordered to assess the progression of the infection. A repeat complete blood count reveals a further increase in white blood cell count to 18,000/mm³, and her serum creatinine has risen to 1.6 mg/dL, indicating worsening renal function. Blood cultures have returned positive for E. coli, confirming bacteremia, a clear sign that the infection has entered the bloodstream, raising the risk of sepsis. The patient's urine output has decreased, and her urine appears darker, suggesting possible acute kidney injury.
These developments necessitate a reassessment of the treatment plan. The medical team considers escalating antibiotic therapy by adding gentamicin to the regimen for broader coverage. Additionally, supportive measures are intensified, including intravenous fluids to maintain renal perfusion and careful monitoring of electrolytes due to the risk of imbalance from decreased renal clearance. The patient's clinical status is critically evaluated through frequent vital signs checks and laboratory tests, with the aim of preventing further deterioration and addressing potential complications such as septic shock.
Section 3
Despite the medical team's efforts, the patient's condition continues to worsen, highlighting the complexity of her case and the need for thorough clinical reasoning. The addition of gentamicin to the antibiotic regimen aimed to broaden the antimicrobial coverage, but within the next 12 hours, the patient's vital signs reveal further instability. Her heart rate has increased to 120 bpm, and her blood pressure has dropped to 100/65 mmHg, indicating a potential progression towards septic shock. The patient's respiratory rate has risen to 24 breaths per minute, and she appears increasingly lethargic, requiring frequent verbal stimulation to maintain alertness.
New laboratory results show an alarming lactic acid level of 3.5 mmol/L, corroborating the suspicion of sepsis due to the compromised perfusion and oxygenation of tissues. Her blood urea nitrogen (BUN) has escalated to 28 mg/dL, further confirming acute kidney injury as a consequence of the ongoing infection and inadequate renal perfusion. The patient's urine output remains low, and continuous monitoring shows a further decline in glomerular filtration rate (GFR), emphasizing the urgent need for a multifaceted intervention strategy.
In response to these developments, the medical team initiates prompt fluid resuscitation with isotonic saline to improve hemodynamic stability and enhance renal perfusion. Additionally, vasopressor support with norepinephrine is considered to address refractory hypotension, while close attention is paid to the balance between fluid overload and effective tissue perfusion. The patient's care is escalated to the intensive care unit for closer monitoring and rapid intervention, underscoring the critical nature of her condition and the necessity for vigilant clinical oversight to prevent further deterioration and potential organ failure.
Section 4
The patient is now in the intensive care unit, where a more comprehensive assessment reveals additional clinical findings that warrant immediate attention. Her skin appears mottled and cool to the touch, indicating poor peripheral perfusion. Despite the initial fluid resuscitation efforts, her urine output remains minimal, at less than 20 mL per hour, suggesting persistent renal compromise. Neurologically, the patient exhibits fluctuating levels of consciousness, alternating between lethargy and agitation. This neurological instability raises concerns about potential cerebral hypoperfusion or the possibility of septic encephalopathy, necessitating continuous monitoring and further neurological evaluation.
New diagnostic results reveal a critical decline in the patient's arterial blood gas (ABG) measurements. The results demonstrate a metabolic acidosis with a pH of 7.28, bicarbonate level of 18 mEq/L, and a base deficit of -7, confirming the presence of severe metabolic derangement likely due to lactic acidosis and renal failure. Additionally, blood cultures reveal a gram-negative bacteremia, providing crucial information for tailoring antibiotic therapy and indicating a more targeted approach may be required to effectively combat the infection. Given these developments, the medical team considers adjusting the antibiotic regimen and potentially incorporating renal replacement therapy to address the worsening kidney function and facilitate clearance of toxins and excess acid from the bloodstream.
The patient's response to the interventions remains closely monitored. Despite the administration of norepinephrine, her mean arterial pressure (MAP) struggles to stabilize above 65 mmHg, pointing to the need for escalating vasopressor support. This indicates a continued risk of septic shock, prompting the healthcare team to explore additional supportive measures, such as the initiation of corticosteroids to manage potential adrenal insufficiency. The integration of a multidisciplinary approach involving infectious disease specialists, nephrologists, and intensivists becomes imperative to navigate the complexities of the patient's evolving condition, ensuring that each intervention is strategically aligned to optimize her chances of recovery while mitigating the risk of further complications.
Section 5
As the medical team intensifies their efforts to stabilize the patient, a change in her status becomes evident. Over the course of the next few hours, her condition further deteriorates with the development of acute respiratory distress syndrome (ARDS). The patient begins to exhibit increased respiratory effort, with a respiratory rate climbing to 32 breaths per minute and oxygen saturation dropping to 85% on a non-rebreather mask. Auscultation of the lungs reveals diffuse crackles, indicative of fluid accumulation and impaired gas exchange. A chest X-ray is promptly obtained, revealing bilateral infiltrates consistent with ARDS, necessitating the initiation of mechanical ventilation to support her failing respiratory system and improve oxygenation.
The patient's hemodynamic status continues to be precarious. Despite the titration of norepinephrine and the addition of vasopressin to address refractory hypotension, her blood pressure remains labile, with systolic readings oscillating between 80-90 mmHg. The persistence of low urine output and elevated serum creatinine, now at 3.2 mg/dL, underscore the severity of her renal impairment. The decision is made to initiate continuous renal replacement therapy (CRRT) to manage her acute kidney injury, address metabolic acidosis, and provide better fluid balance. This intervention aims to prevent further accumulation of toxins and support her hemodynamic stability.
With these developments, the interdisciplinary team continues to strategize the patient's management plan. The intensivists, in collaboration with the nephrologists and pulmonologists, re-evaluate her ventilator settings and renal support protocols, ensuring optimal delivery of care. Concurrently, the infectious disease specialists refine her antibiotic regimen based on the sensitivity results of the blood cultures, aiming for more targeted antimicrobial therapy. The team remains vigilant, anticipating potential complications such as disseminated intravascular coagulation (DIC) and monitoring for signs of multi-organ dysfunction. The complexity of the patient's condition demands a coordinated and dynamic approach, with ongoing assessments and timely interventions to navigate the critical phases of her illness and improve her prognosis.