Pyelonephritis - Nursing Case Study

Pathophysiology

• Primary mechanism: Bacterial ascent from the lower urinary tract, often E. coli, leads to infection of the renal pelvis and parenchyma. This ascent is facilitated by vesicoureteral reflux or obstruction, promoting bacterial colonization.

• Secondary mechanism: Inflammatory response characterized by neutrophil infiltration and cytokine release, causing renal tissue damage and impaired function. This response can lead to interstitial edema and tubular necrosis, further exacerbating kidney injury.

• Key complication: If untreated, the infection can progress to chronic pyelonephritis, leading to scarring, hypertension, and even renal failure. Early recognition and treatment are crucial to prevent these serious outcomes.

Patient Profile

Demographics:

35-year-old female, nurse

History:

• Key past medical history: History of recurrent urinary tract infections, hypertension

• Current medications: Lisinopril 10 mg daily, ibuprofen as needed

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe lower back pain and fever

• Key symptoms: Nausea, vomiting, chills, dysuria, increased urinary frequency, and flank pain

• Vital signs: Temperature 102.5°F (39.2°C), heart rate 110 bpm, blood pressure 140/90 mmHg, respiratory rate 22 breaths per minute

Section 1

As the healthcare team conducts an initial assessment, the patient's presentation suggests a severe case of pyelonephritis with potential complications. Her physical examination reveals right-sided costovertebral angle tenderness, indicating significant inflammation of the kidney. The palpable tenderness, combined with her high fever and tachycardia, raises concerns about the severity of the infection. Laboratory tests are promptly ordered, including a complete blood count (CBC), urinalysis, blood cultures, and renal function tests. The urinalysis shows significant pyuria and bacteriuria, with white blood cell casts indicating upper urinary tract involvement. Blood cultures are pending, but initial results from the CBC reveal leukocytosis with a left shift, indicating an acute bacterial infection. Serum creatinine and blood urea nitrogen (BUN) levels are slightly elevated, suggesting impaired renal function potentially due to interstitial edema and inflammatory damage.

Despite initial hydration therapy and broad-spectrum intravenous antibiotics, the patient's condition deteriorates. She begins to exhibit signs of systemic inflammatory response syndrome (SIRS), as evidenced by persistent tachycardia, hypotension (blood pressure now at 100/60 mmHg), and increased respiratory rate of 26 breaths per minute. Additionally, her fever remains high, and she reports increasing confusion and lethargy, suggesting potential progression to sepsis. The healthcare team recognizes the need for urgent intervention to prevent further complications such as septic shock or acute kidney injury.

Given these developments, the team decides to escalate care by transferring the patient to the intensive care unit (ICU) for closer monitoring and aggressive management. A nephrology consult is requested to evaluate for possible acute kidney injury and to guide further treatment. The patient's worsening clinical status underscores the need for a multidisciplinary approach, integrating infection control, hemodynamic support, and renal protective strategies to optimize outcomes and prevent further deterioration.

Section 2

Following the transfer to the ICU, the healthcare team initiates a more aggressive management plan to address the patient's deteriorating condition. Continuous cardiac monitoring reveals a persistently elevated heart rate of 125 beats per minute, and her blood pressure has further declined to 92/58 mmHg, indicating worsening hemodynamic instability. Despite the administration of intravenous fluids, her urine output has decreased to 20 mL/hour, suggesting oliguria and potential progression towards acute kidney injury (AKI). In response, the team initiates vasopressor support with norepinephrine to address her hypotension and improve renal perfusion.

The nephrology consult recommends additional renal function tests and a renal ultrasound to assess for any obstructive causes contributing to her AKI. The ultrasound reveals mild hydronephrosis, likely secondary to inflammation, but no obstructing calculi are identified. Meanwhile, repeat laboratory tests show a further increase in serum creatinine to 2.1 mg/dL and BUN levels rising to 32 mg/dL, reinforcing concerns about declining renal function. Lactate levels are elevated at 3.2 mmol/L, indicative of tissue hypoperfusion and raising the suspicion of evolving septic shock.

The healthcare team convenes to reassess the treatment plan, emphasizing the need to titrate antibiotics based on pending culture sensitivities and to optimize fluid management to balance hemodynamic support and renal protection. The patient's increasing confusion and lethargy necessitate close neurological monitoring and consideration of adjunctive therapies to mitigate the risk of further complications. The multidisciplinary approach continues to be crucial, as the team aims to stabilize the patient and prevent the progression to severe organ dysfunction.

Section 3

As the healthcare team continues to monitor the patient closely, her condition begins to show signs of further complications. Over the next few hours, despite the ongoing vasopressor support and antibiotic therapy, her blood pressure remains only partially responsive, fluctuating between 90/55 mmHg and 95/60 mmHg. The persistent hypotension raises concerns about the adequacy of perfusion to vital organs. Her heart rate climbs to 130 beats per minute, indicating sustained tachycardia and the body's ongoing struggle to maintain hemodynamic stability.

New diagnostic results arrive, revealing a critical drop in hemoglobin to 8.5 g/dL and hematocrit to 25%, suggesting possible hemolysis or an underlying bleeding issue. Additionally, her platelet count has decreased to 110,000/mm³, raising the suspicion of evolving disseminated intravascular coagulation (DIC) as a complication of sepsis. The rising lactate level, now at 4.0 mmol/L, further confirms the presence of significant tissue hypoxia and metabolic acidosis.

In light of these developments, the team decides to initiate a red blood cell transfusion to address the anemia and improve oxygen delivery. Concurrently, they adjust her antibiotic regimen based on preliminary culture results, which indicate the presence of a resistant strain of Escherichia coli. This adjustment is critical as they aim to target the infection more effectively. With her mental status remaining altered, neurological assessments are prioritized to monitor for any signs of cerebral compromise. The team remains vigilant, recognizing the need for continuous reassessment and timely interventions to prevent the progression to multi-organ failure. The emphasis on a coordinated multidisciplinary approach remains paramount as the patient navigates this critical phase of her illness.

Section 4

As the healthcare team continues to monitor the patient, they observe a change in her status that prompts immediate attention. Her respiratory rate has increased to 28 breaths per minute, and she is exhibiting signs of respiratory distress, including nasal flaring and the use of accessory muscles. Arterial blood gas analysis reveals a pH of 7.32, a PaCO2 of 48 mmHg, and a PaO2 of 60 mmHg, indicating a worsening respiratory acidosis and hypoxemia. This respiratory compromise suggests a potential progression of sepsis-related acute respiratory distress syndrome (ARDS), requiring urgent intervention.

Despite the red blood cell transfusion, the patient remains lethargic with a Glasgow Coma Scale score of 10, indicating a continued risk of neurological deterioration. Her pupils are sluggishly reactive, and there is a noticeable delay in her response to verbal stimuli. The neurological team is consulted to evaluate the need for further imaging, such as a CT scan, to rule out any intracranial pathology that may be contributing to her altered mental state.

The team decides to escalate respiratory support by initiating non-invasive positive pressure ventilation to improve oxygenation and reduce the work of breathing. They continue to monitor her hemodynamics closely, particularly in light of the suspected DIC, which complicates her condition. As the patient's journey becomes increasingly complex, the team's coordinated approach remains crucial, balancing the need for aggressive treatment of sepsis and its complications while maintaining vigilance for further changes in her clinical status. The multidisciplinary collaboration is essential to navigate this critical phase, with the goal of stabilizing the patient and preventing further progression to multi-organ failure.

Section 5

As the healthcare team continues to manage the patient, they notice a change in her status that demands immediate reassessment. The patient's blood pressure has dropped to 88/54 mmHg, her heart rate has increased to 122 beats per minute, and her temperature has spiked to 39.5°C. These signs suggest a progression to septic shock, a serious complication of her initial pyelonephritis. Her skin appears mottled, and capillary refill is delayed, indicating poor perfusion. The clinical team prioritizes fluid resuscitation with isotonic crystalloids to address hypoperfusion and support her blood pressure. Simultaneously, broad-spectrum antibiotics are continued to manage the underlying infection.

New laboratory results reveal a significant drop in platelet count to 75,000/mm³, further supporting the suspicion of disseminated intravascular coagulation (DIC), a complication that aligns with her worsening condition. The team decides to initiate low-dose heparin therapy cautiously, balancing the risk of hemorrhage with the need to prevent further thrombotic events. A repeat arterial blood gas analysis shows a pH of 7.28, PaCO2 of 52 mmHg, and PaO2 of 55 mmHg, confirming ongoing respiratory acidosis and worsening hypoxemia despite non-invasive ventilation. The respiratory therapist suggests re-evaluating the current respiratory support strategy, considering the potential need for intubation and mechanical ventilation to stabilize her rapidly declining respiratory status.

As the patient's condition evolves, the team implements continuous renal replacement therapy (CRRT) to manage acute kidney injury secondary to sepsis and DIC, aiming to stabilize her metabolic status and manage fluid overload. The collaborative efforts of the multidisciplinary team remain critical as they strategize to prevent the progression to multi-organ dysfunction syndrome (MODS). The team prepares to reassess her neurological status and hemodynamics continually, ensuring any further deterioration is promptly addressed, with the ultimate goal of guiding her towards recovery while minimizing the risk of additional complications.