sepsis - Nursing Case Study
Pathophysiology
• Primary mechanism: Dysregulated host response to infection leads to widespread inflammation, causing damage to tissues and organs. This systemic inflammatory response is driven by cytokine release, which increases vascular permeability and leads to hypotension and tissue hypoperfusion.
• Secondary mechanism: Coagulation cascade activation results in microthrombi formation. This impairs blood flow, exacerbating organ dysfunction. Simultaneously, the consumption of clotting factors and platelets contributes to disseminated intravascular coagulation, further complicating the clinical picture.
• Key complication: Multi-organ dysfunction syndrome (MODS) occurs as a result of impaired oxygen delivery and persistent inflammation, leading to failure of critical systems, such as renal, hepatic, and respiratory functions, which significantly increases morbidity and mortality in septic patients.
Patient Profile
Demographics:
56-year-old female, school teacher
History:
• Key past medical history: Hypertension, type 2 diabetes
• Current medications: Lisinopril, Metformin, Atorvastatin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Fever and confusion
• Key symptoms: Increased heart rate, low urine output, chills, fatigue
• Vital signs: Temperature 38.9°C (102°F), heart rate 115 bpm, blood pressure 92/58 mmHg, respiratory rate 24 breaths per minute, oxygen saturation 93% on room air
Section 1
As the healthcare team continues to monitor the patient, her condition reveals further complications indicative of progressing sepsis. During the initial assessment in the ICU, the patient's urine output remains critically low, with less than 30 mL in the past two hours, suggesting acute kidney injury. Her skin appears cool and clammy, and capillary refill time is prolonged, indicating poor peripheral perfusion. Auscultation of the lungs reveals bilateral crackles, raising concerns about pulmonary edema, possibly due to fluid overload and impaired cardiac function. Given her history of hypertension and diabetes, her cardiovascular system is particularly vulnerable, exacerbating her hypotension and increasing the risk of cardiogenic shock.
New diagnostic results further illuminate the patient's deteriorating state. Her complete blood count shows leukocytosis, with a white blood cell count of 18,000/mm³, and a left shift, which is typical in systemic infections. Renal function tests reveal elevated creatinine levels at 2.5 mg/dL and blood urea nitrogen (BUN) at 45 mg/dL, confirming acute kidney injury. Liver function tests are also abnormal, with elevated bilirubin and transaminases, suggesting hepatic involvement. An arterial blood gas analysis shows metabolic acidosis with a pH of 7.32 and a bicarbonate level of 18 mEq/L, indicating impaired acid-base balance due to lactic acidosis from poor tissue perfusion.
The healthcare team faces a critical juncture in the patient's care, requiring immediate interventions to stabilize her condition and prevent further organ damage. The next steps will involve aggressive fluid resuscitation while monitoring for fluid overload, initiation of broad-spectrum antibiotics tailored to her penicillin allergy, and consideration of vasopressor support to maintain hemodynamic stability. Close monitoring of her renal and hepatic function, along with respiratory support, will be essential in navigating this complex clinical scenario. The emerging picture of multi-organ dysfunction necessitates a coordinated, multi-disciplinary approach to optimize outcomes and mitigate the risks of further complications.
Section 2
Change in Patient Status
As the healthcare team implements the initial interventions to stabilize the patient, her condition remains tenuous, and close monitoring of her vital signs reveals concerning trends. Despite aggressive fluid resuscitation efforts, her blood pressure continues to hover at a low mean arterial pressure of 60 mmHg, necessitating the initiation of norepinephrine to support her hemodynamic status. Her heart rate remains elevated at 120 beats per minute, indicating persistent tachycardia as her body struggles to compensate for the hypotension. The patient exhibits signs of respiratory distress, with an increased respiratory rate of 28 breaths per minute and an oxygen saturation that has decreased to 88% on supplemental oxygen. These findings suggest worsening pulmonary involvement, likely due to fluid accumulation and impaired gas exchange.
In response to the declining respiratory status, the team decides to initiate non-invasive positive pressure ventilation to improve oxygenation and reduce the work of breathing. Meanwhile, the patient's urine output remains concerningly low, with only 10 mL in the last hour, reinforcing the gravity of the acute kidney injury. The lab results reveal that her serum lactate level has risen further to 4.5 mmol/L, highlighting ongoing tissue hypoxia and the need for continued reassessment of the fluid management strategy to balance the risks of fluid overload with the necessity of maintaining adequate perfusion.
The patient’s persistent metabolic acidosis, now with a pH of 7.28, underscores the urgency of the situation as the team contemplates additional interventions to correct the acid-base imbalance. With the threat of multi-organ dysfunction looming, the healthcare team must continuously evaluate the efficacy of current treatments and remain vigilant for any signs of further deterioration. The collaborative efforts of the critical care team, including intensivists, nephrologists, and respiratory therapists, are crucial as they navigate the complexities of sepsis management to prevent further complications and improve the patient’s chances of recovery.
Section 3
As the healthcare team closely monitors the patient’s progress, new diagnostic results reveal significant insights into her condition. A chest X-ray confirms bilateral infiltrates consistent with acute respiratory distress syndrome (ARDS), explaining her worsening respiratory status and hypoxemia despite non-invasive ventilation. This finding necessitates a multidisciplinary discussion regarding the potential need for intubation and mechanical ventilation to ensure adequate oxygenation and prevent respiratory failure. Additionally, an echocardiogram is performed to assess cardiac function, revealing a reduced ejection fraction of 35%, indicative of septic cardiomyopathy. This cardiac dysfunction further complicates fluid management, as the team must now carefully titrate fluids and vasopressors to support both cardiac output and systemic perfusion.
Concurrently, a repeat set of laboratory tests shows the patient’s renal function continues to decline, with serum creatinine rising to 2.8 mg/dL and blood urea nitrogen (BUN) at 45 mg/dL, confirming the progression of acute kidney injury. Given the oliguria and electrolyte imbalances, including hyperkalemia with a potassium level of 5.8 mmol/L, the possibility of initiating renal replacement therapy is considered to manage fluid overload and correct metabolic derangements. The nephrology team evaluates the patient for potential dialysis, balancing the risks of invasive intervention against the necessity of preventing further renal and systemic complications.
These developments prompt the healthcare team to reassess the overall management strategy, prioritizing stabilization of respiratory and cardiac function, while carefully monitoring renal output and adjusting interventions accordingly. The complexity of the patient’s condition underscores the importance of ongoing interdisciplinary collaboration and dynamic clinical reasoning to adapt to the evolving clinical picture. As the team prepares for potential escalation of care, they remain vigilant for any signs of further deterioration, aiming to mitigate the risk of multi-organ dysfunction and improve the patient’s trajectory toward recovery.
Section 4
As the healthcare team proceeds with the management plan, they closely monitor the patient's response to the interventions. The decision to intubate and initiate mechanical ventilation is made to address her severe hypoxemia and prevent respiratory failure. Post-intubation, her arterial blood gas results show improved oxygenation, with a PaO2 of 75 mmHg and a PaCO2 of 45 mmHg on a FiO2 of 60%. Her work of breathing decreases, and her oxygen saturation stabilizes at 94%, suggesting a positive response to mechanical ventilation. However, her hemodynamic status remains tenuous. Despite cautious fluid administration and low-dose norepinephrine to maintain mean arterial pressure, her blood pressure hovers at 88/55 mmHg, indicating continued vasodilation and cardiac compromise from septic shock.
Further complicating her clinical picture, the patient's urine output drops to less than 20 mL/hour over the next 6 hours, and her serum potassium rises to 6.2 mmol/L, raising concerns about severe hyperkalemia. An urgent nephrology consult leads to the initiation of continuous renal replacement therapy (CRRT) to manage electrolyte imbalances and provide renal support. The team carefully monitors her electrolyte levels, aiming to decrease the potassium level to below 5 mmol/L and stabilize her renally-driven acid-base status. Her serum lactate remains elevated at 4.5 mmol/L, indicating ongoing tissue hypoperfusion and highlighting the need for continued vigilance in her resuscitation.
As the patient's care continues, the team remains focused on assessing potential signs of further deterioration, particularly the risk of multi-organ dysfunction. The interdisciplinary team discusses the need for potential escalation of vasopressor therapy and titration of ventilatory support to optimize her hemodynamic status and oxygen delivery. They also consider the possibility of adjunctive therapies, such as corticosteroids, to address refractory septic shock. The situation demands dynamic clinical reasoning and rapid decision-making to navigate the complexities of her condition and steer her toward recovery. The team remains hopeful but prepared for the challenges of managing the interplay between her respiratory, cardiac, and renal dysfunctions.
Section 5
As the healthcare team continues to monitor the patient's progress, new diagnostic results emerge that provide additional insights into her condition. A follow-up echocardiogram reveals moderate left ventricular dysfunction with an ejection fraction of 35%, suggesting that septic cardiomyopathy may be contributing to her hemodynamic instability. This finding prompts the team to consider the addition of inotropic support with dobutamine to enhance cardiac output and improve tissue perfusion. Meanwhile, a repeat chest X-ray shows bilateral infiltrates, consistent with acute respiratory distress syndrome (ARDS), reinforcing the need for careful management of her ventilatory settings to balance oxygenation with lung protection strategies.
In the context of these findings, the patient's condition presents a complex interplay of septic shock, evolving cardiac compromise, and respiratory failure. Her laboratory results continue to reflect this precarious balance, with a slight improvement in serum lactate to 3.8 mmol/L, yet persistent mild metabolic acidosis with a bicarbonate level of 18 mmol/L. The team discusses the potential benefits and risks of initiating low-dose corticosteroids to address refractory shock, weighing the possibility of improved hemodynamic stability against the risk of immunosuppression in the setting of sepsis.
Amidst these challenges, the team observes a modest improvement in the patient's urine output, now at 30 mL/hour, as CRRT continues to support her renal function. The interdisciplinary team remains vigilant, recognizing that while certain parameters show signs of stabilization, the risk of further complications persists. Their focus remains on iterative assessments and timely adjustments to her management plan, aiming to optimize her recovery trajectory while remaining prepared to address any new developments in her clinical status.