Sepsis - Nursing Case Study
Pathophysiology
• Primary mechanism: Sepsis begins with an overwhelming immune response to infection, where pro-inflammatory cytokines are released excessively, leading to systemic inflammation and endothelial cell activation. This process results in increased vascular permeability and vasodilation, causing hypotension and tissue hypoperfusion.
• Secondary mechanism: The inflammatory cascade also triggers the coagulation system, causing disseminated intravascular coagulation (DIC). This leads to widespread microthrombi formation, which further impairs blood flow and exacerbates organ dysfunction due to ischemia.
• Key complication: The combination of systemic inflammation, abnormal coagulation, and impaired perfusion can progress to multiple organ dysfunction syndrome (MODS), where organs such as the lungs, kidneys, and liver fail to function properly, significantly increasing morbidity and mortality.
Patient Profile
Demographics:
57-year-old female, school teacher
History:
• Key past medical history: Type 2 diabetes, hypertension
• Current medications: Metformin 500 mg twice daily, Lisinopril 10 mg once daily
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Fever and difficulty breathing
• Key symptoms: High fever, chills, rapid breathing, confusion, low urine output
• Vital signs: Temperature 39.2°C (102.6°F), Heart rate 110 bpm, Respiratory rate 28 breaths per minute, Blood pressure 88/54 mmHg, Oxygen saturation 91% on room air
Section 1
As the medical team conducts an initial assessment, they find that the patient is experiencing increased confusion, indicating potential cerebral hypoperfusion. Her skin appears cool and mottled, particularly in the extremities, which raises concerns about further circulatory compromise. Lung auscultation reveals crackles bilaterally, suggesting fluid accumulation, possibly due to acute respiratory distress syndrome (ARDS), a common complication of sepsis. The team notes that her respiratory effort is labored, and despite being placed on supplemental oxygen via a nasal cannula at 4 liters per minute, her oxygen saturation remains at 92%.
Laboratory results return, showing a white blood cell count of 18,000/mm³, indicating a likely bacterial infection. Her serum lactate level is elevated at 4.5 mmol/L, suggesting tissue hypoxia and indicating the need for aggressive fluid resuscitation. Additionally, her blood cultures are pending, but initial urinalysis shows significant pyuria and bacteriuria, indicating a possible urinary tract infection as the source of sepsis. Her kidney function is deteriorating, with serum creatinine rising to 2.0 mg/dL from a baseline of 1.0 mg/dL, reflecting acute kidney injury. The team decides to escalate care, initiating broad-spectrum antibiotics, excluding penicillin, and increasing intravenous fluid administration to improve perfusion.
Despite these interventions, the patient's blood pressure remains low, and she is started on a norepinephrine infusion to support her hemodynamics. Her urine output is still minimal, raising concerns about progressing renal failure. The team must now consider additional strategies, such as advanced hemodynamic monitoring and potentially dialysis, to manage her worsening condition. This situation prompts a re-evaluation of her care plan and necessitates close monitoring for any signs of further organ dysfunction, particularly in light of her diabetes and hypertension, which could complicate her recovery.
Section 2
As the team continues to monitor the patient, new diagnostic results reveal further insights into her condition. The pending blood cultures return positive for Escherichia coli, confirming the urinary tract infection as the source of sepsis. This information allows the team to adjust the antibiotic regimen to include ceftriaxone, which is effective against this pathogen, thereby optimizing the treatment plan to target the identified infection.
Concurrently, a repeat serum lactate level remains elevated at 4.2 mmol/L, indicating ongoing tissue hypoperfusion despite aggressive fluid resuscitation. Her blood pressure, supported by norepinephrine, is stabilizing at 95/60 mmHg; however, her oxygen saturation has decreased to 89% on the current supplemental oxygen setup. Chest X-ray results show worsening bilateral infiltrates, consistent with evolving ARDS, necessitating an increase in respiratory support. The team considers transitioning her to non-invasive ventilation to improve oxygenation and decrease the work of breathing.
Clinically, the patient's urine output has not improved, with only 150 mL produced over the past 8 hours, further suggesting significant renal compromise. The nephrology team is consulted to evaluate the need for renal replacement therapy. The patient's diabetes and hypertension complicate her management, necessitating careful titration of medications to avoid exacerbating her renal and respiratory instability. The healthcare team remains vigilant, closely monitoring her vital signs and laboratory parameters to swiftly address any further deterioration. Each step in her care is crucial to preventing progression to multiple organ dysfunction syndrome, a significant risk given her current trajectory.
Section 3
As the healthcare team closely monitors the patient's condition, new complications arise that further challenge her management. Despite adjustments to the treatment regimen, the patient's clinical status changes, indicating a potential progression towards multiple organ dysfunction. Over the next few hours, her respiratory status continues to decline. Her oxygen saturation falls to 85% even with the increased support of non-invasive ventilation. Auscultation reveals diminished breath sounds and fine crackles, particularly in the lower lung fields. This suggests worsening pulmonary edema or additional consolidation, complicating the management of her acute respiratory distress syndrome (ARDS).
Laboratory results reveal a concerning trend in her renal function. Her creatinine levels have increased to 3.2 mg/dL from a baseline of 1.1 mg/dL, and her blood urea nitrogen (BUN) has risen to 48 mg/dL, confirming significant acute kidney injury. This renal deterioration coincides with a further drop in urine output to 100 mL over the next 8 hours. Nephrology advises initiation of continuous renal replacement therapy (CRRT) to manage her fluid overload and prevent further renal compromise. Additionally, the patient's blood glucose levels have become more challenging to control, with readings oscillating between 180 mg/dL and 300 mg/dL, despite adjustments to her insulin regimen. This labile glycemic control adds another layer of complexity to her care, requiring frequent monitoring and careful insulin titration.
In response to these changes, the interdisciplinary team holds a critical care conference to reassess the patient's management plan. They consider escalating her respiratory support to invasive mechanical ventilation to ensure adequate gas exchange and decrease her work of breathing. The team also discusses the potential benefits and risks of initiating CRRT, weighing the need for renal support against the risk of further hemodynamic instability. They remain vigilant for any signs of new organ dysfunction, mindful that timely and coordinated interventions are crucial in preventing further deterioration and improving the patient's overall prognosis.
Section 4
As the interdisciplinary team proceeds with the decision to transition the patient to invasive mechanical ventilation, they carefully prepare her for intubation, ensuring sedation and analgesia are adequately managed to prevent distress. Once intubated, her ventilator settings are optimized for protective lung strategy, focusing on low tidal volumes and adequate positive end-expiratory pressure (PEEP) to mitigate further lung injury. Despite these adjustments, her blood gas analysis reveals a persistent respiratory acidosis, with a pH of 7.28 and a PaCO2 of 55 mmHg, indicating the need for ongoing close monitoring and potential ventilatory support adjustments.
Simultaneously, CRRT is initiated to address her acute kidney injury and fluid overload. The nephrology team selects a continuous venovenous hemofiltration (CVVH) mode, balancing fluid removal with hemodynamic stability. Over the next 12 hours, there is a modest improvement in her fluid status, as evidenced by a slight decrease in her central venous pressure (CVP) from 14 mmHg to 11 mmHg. However, her blood pressure remains labile, with readings fluctuating between 85/50 mmHg and 95/55 mmHg, necessitating the continuation of vasopressor support to maintain adequate perfusion.
Despite these interventions, the team notes new complications emerging. Her liver function tests reveal a rising trend, with her AST climbing to 152 U/L and ALT to 145 U/L, suggesting the onset of hepatic dysfunction. Her total bilirubin has also increased to 3.5 mg/dL, raising concerns about progressing toward multi-organ dysfunction syndrome (MODS). The team recognizes the need to further investigate potential causes, such as drug-induced liver injury or ischemic hepatitis, while maintaining vigilance for any additional signs of deterioration. These developments prompt an urgent reevaluation of her current treatment strategy, emphasizing the importance of a dynamic and responsive approach to her critical care management.
Section 5
As the interdisciplinary team continues to monitor the patient closely, they note a change in her status that demands immediate attention. Overnight, the nurse caring for her observes increased agitation and restlessness, despite adequate sedation and analgesia. Her heart rate has risen to 130 beats per minute, and her blood pressure has further decreased to 80/45 mmHg, even with the ongoing vasopressor support. This worrisome trend suggests that she may be experiencing further hemodynamic instability.
The medical team swiftly convenes to assess potential causes for this deterioration. A repeat blood gas analysis shows worsening respiratory acidosis, with a pH now at 7.25 and a PaCO2 of 60 mmHg, indicating possible ventilatory support inadequacy. Additionally, her lactate levels have risen to 5.0 mmol/L, pointing to increased tissue hypoperfusion and raising the possibility of evolving septic shock. Given these findings, the team decides to escalate her vasopressor therapy and consider the need for additional inotropic support to improve her cardiac output and tissue perfusion.
In parallel, the team recognizes the importance of re-evaluating her sedation regimen to balance between adequate sedation and the risk of further hemodynamic compromise. They also plan to repeat imaging studies, including an abdominal ultrasound, to explore any new or worsening intra-abdominal issues that might be contributing to her liver dysfunction and overall instability. These steps are crucial as they continue to navigate the complexities of her critical condition, underscoring the necessity of a dynamic and multifaceted approach to her care.