Sepsis - Nursing Case Study

Pathophysiology

• Primary mechanism: Sepsis begins with a dysregulated immune response to an infection, leading to widespread inflammation. This excessive response causes the release of pro-inflammatory cytokines, which damage tissues and organs.

• Secondary mechanism: The inflammatory cascade disrupts the endothelial barrier, causing increased vascular permeability. This results in fluid leakage into tissues, leading to hypotension and impaired organ perfusion.

• Key complication: As the condition progresses, the combination of systemic inflammation and poor perfusion can lead to multiple organ dysfunction syndrome (MODS), characterized by the failure of vital organs such as the kidneys, lungs, and heart.

Patient Profile

Demographics:

56-year-old female, teacher

History:

• Key past medical history: Type 2 Diabetes, Hypertension

• Current medications: Metformin, Lisinopril, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Fever and confusion

• Key symptoms: Elevated heart rate, shortness of breath, decreased urine output, chills

• Vital signs: Temperature 39.2°C (102.6°F), Heart rate 118 bpm, Respiratory rate 24 breaths/min, Blood pressure 88/56 mmHg, Oxygen saturation 92% on room air

Section 1

As the healthcare team continues to assess the 56-year-old female patient, further diagnostic tests are conducted to better understand the underlying causes of her sepsis and to monitor her condition. Blood cultures are obtained to identify the source of infection, and a complete blood count (CBC) reveals leukocytosis with a white blood cell count of 18,000 cells/mm³, indicating a significant inflammatory response. Additionally, the patient's blood glucose level is elevated at 240 mg/dL, likely exacerbated by the physiological stress of infection and her history of type 2 diabetes. A chest X-ray is performed, revealing bilateral infiltrates suggestive of pneumonia, which may be the primary source of her septic state.

In the course of treatment, the patient is started on a broad-spectrum antibiotic regimen, excluding penicillin due to her allergy. Fluid resuscitation with intravenous crystalloids is initiated to address hypotension and improve tissue perfusion. Despite these interventions, her blood pressure remains low, and her urine output continues to decrease, raising concerns about acute kidney injury (AKI) as a new complication. Serum creatinine levels are found to be elevated at 2.1 mg/dL, confirming the suspicion of renal impairment.

Clinicians must now consider the next steps in managing her condition, such as the potential need for vasopressor support to maintain adequate blood pressure and perfusion. The interdisciplinary team also reviews her medication regimen to ensure optimal glycemic control, given her elevated blood glucose, which could further impact her immune response and recovery. As the patient's condition evolves, continuous monitoring and reassessment are crucial to adapt the treatment plan, prevent further complications, and guide the transition to more targeted therapies once the specific pathogen is identified.

Section 2

As the healthcare team continues to monitor the 56-year-old female patient, her condition begins to show signs of further deterioration despite ongoing treatment efforts. Her blood pressure remains persistently low, with readings hovering around 86/54 mmHg, and her heart rate has increased to 120 beats per minute, indicating a compensatory response to hypotension. Her respiratory rate has also risen to 28 breaths per minute, and she is exhibiting increased work of breathing. These changes suggest that the patient is not adequately responding to fluid resuscitation, and there is a growing concern for septic shock, which necessitates urgent intervention.

In light of these worrying developments, the healthcare team decides to initiate vasopressor therapy with norepinephrine to support her blood pressure and improve tissue perfusion. Concurrently, they adjust her insulin regimen to bring her blood glucose levels under tighter control, with the current reading at 260 mg/dL, which could potentially exacerbate her inflammatory response and complicate her recovery. The team also considers the possibility of acute respiratory distress syndrome (ARDS) given her bilateral infiltrates and worsening respiratory status, prompting the initiation of supplemental oxygen therapy to maintain adequate oxygen saturation levels, currently recorded at 89% on room air.

As the patient receives these additional interventions, the interdisciplinary team prepares for the next steps, which include continuous reassessment of her hemodynamic status, respiratory function, and renal parameters. The plan also involves awaiting the results of blood cultures to tailor antibiotic therapy more specifically to the identified pathogen, thereby optimizing her treatment. The focus remains on stabilizing her condition, preventing further complications, and transitioning her to a recovery phase once she shows signs of improvement.

Section 3

As the interdisciplinary team continues to monitor the patient, new diagnostic results bring both clarity and additional concerns. The blood cultures return positive for Escherichia coli, indicating a gram-negative bacteremia that is likely the source of her sepsis. This finding necessitates an adjustment in her antibiotic regimen to include a more targeted therapy, such as piperacillin-tazobactam, in order to effectively combat the identified pathogen. Despite these targeted interventions, the patient's condition remains critical.

Further diagnostic imaging reveals worsening bilateral pulmonary infiltrates, consistent with the development of acute respiratory distress syndrome (ARDS). Her oxygen saturation continues to decline, now at 85% despite supplemental oxygen via a non-rebreather mask. The respiratory therapist suggests transitioning to high-flow nasal cannula or considering non-invasive ventilation to improve her oxygenation status. The team also notes an increase in her lactate levels to 3.8 mmol/L, suggesting ongoing tissue hypoperfusion and highlighting the need for continued hemodynamic support.

The nephrology consult reveals early signs of acute kidney injury, with her serum creatinine rising to 2.1 mg/dL from a baseline of 1.0 mg/dL, reflecting compromised renal function likely due to both hypoperfusion and nephrotoxic effects of medications. The team discusses the potential need for renal replacement therapy if her renal function continues to decline. Faced with these complications, the healthcare team remains vigilant, prioritizing supportive care and frequent reassessment to adapt the treatment plan as needed, aiming to stabilize her condition and prevent further deterioration.

Section 4

As the interdisciplinary team continues its vigilant care, the patient's condition presents a concerning new complication. Over the next 12 hours, despite the initiation of high-flow nasal cannula to improve oxygenation, her respiratory status deteriorates further. Her oxygen saturation drops to 82%, even with the increased support, and she begins to exhibit increased work of breathing, characterized by rapid, shallow respirations at a rate of 32 breaths per minute. Auscultation reveals diminished breath sounds bilaterally with diffuse crackles, indicative of fluid accumulation and worsening ARDS. The decision is made to escalate respiratory support to non-invasive ventilation, with a close watch for signs of respiratory fatigue that may necessitate intubation.

Concurrently, the patient's hemodynamic status raises additional concerns. Her blood pressure trends downward to 88/54 mmHg, despite ongoing fluid resuscitation and vasopressor support with norepinephrine. This hypotension, coupled with persistent tachycardia at 118 beats per minute, suggests worsening septic shock. The interdisciplinary team, including the intensivist, considers optimizing her hemodynamic management, potentially adding a second vasopressor such as vasopressin to stabilize her blood pressure. They also explore the possibility of escalating fluid management strategies, balancing the risk of fluid overload against the need to improve perfusion.

Meanwhile, her renal function continues to decline, with serum creatinine now at 2.5 mg/dL and urine output decreasing to less than 30 mL/hour, meeting the criteria for stage 2 acute kidney injury. These findings prompt further discussion about initiating renal replacement therapy to support her compromised kidney function. The team acknowledges that this intervention could aid in managing her fluid status and electrolyte balance, which is critical given her tenuous condition. As the team navigates these complex clinical challenges, they remain committed to adapting the treatment plan, leveraging their collective expertise to stabilize the patient and prevent further deterioration.

Section 5

As the team continues to provide comprehensive care, new diagnostic results from the latest arterial blood gas analysis reveal concerning changes. The patient's PaO2 has decreased to 55 mmHg, confirming significant hypoxemia despite the use of non-invasive ventilation. Her PaCO2 has risen to 48 mmHg, indicating impending respiratory acidosis, and her pH has dropped to 7.28, further underscoring the development of respiratory failure. The lactate level has increased to 4.5 mmol/L, reflecting ongoing tissue hypoperfusion and metabolic acidosis linked to her septic state. These findings necessitate an urgent multidisciplinary discussion to reassess her respiratory support and hemodynamic management strategies.

In light of these diagnostic results, the team decides to proceed with intubation and mechanical ventilation to better support her deteriorating respiratory status and improve oxygenation. They prepare for this transition by ensuring all necessary equipment and medications are ready, while continuing to monitor her hemodynamic stability. The addition of vasopressin is initiated to address the refractory hypotension, with careful titration to maintain a mean arterial pressure above 65 mmHg.

Amidst these interventions, the patient's neurological status begins to change. She becomes increasingly lethargic and less responsive to verbal stimuli, raising concerns about potential encephalopathy secondary to severe sepsis. This prompts an evaluation to rule out other causes, such as hypoxemia or medication effects, while ensuring her safety with continuous monitoring. The team remains vigilant, adapting their approach to the evolving challenges, determined to improve her trajectory and mitigate further deterioration as they await the effects of the new interventions.