sepsis - Nursing Case Study
Pathophysiology
• Primary mechanism: Dysregulated immune response - Sepsis begins with an infection that triggers the immune system to release inflammatory mediators excessively. This uncontrolled response can damage tissues and organs, leading to systemic inflammation and potential organ dysfunction.
• Secondary mechanism: Endothelial dysfunction - Inflammation causes the endothelial cells lining blood vessels to become activated and damaged. This leads to increased vascular permeability and the leakage of fluids into surrounding tissues, contributing to hypotension and impaired blood flow to organs.
• Key complication: Disseminated Intravascular Coagulation (DIC) - The inflammatory response can activate the coagulation cascade, causing widespread clot formation and consumption of clotting factors. This increases the risk of bleeding and can exacerbate organ damage, complicating recovery and treatment.
Patient Profile
Demographics:
48-year-old female, school teacher
History:
• Key past medical history: Hypertension, type 2 diabetes, previous urinary tract infections
• Current medications: Metformin, Lisinopril, Aspirin
• Allergies: Penicillin
Current Presentation:
• Chief complaint: Fever and confusion
• Key symptoms: High fever, increased heart rate, confusion, difficulty breathing, decreased urine output
• Vital signs: Temperature 102.5°F, heart rate 115 bpm, respiratory rate 24 breaths per minute, blood pressure 90/60 mmHg, oxygen saturation 92% on room air
Section 1
As the medical team proceeds with the initial assessment, the clinical picture becomes more concerning. Physical examination reveals cool, clammy skin and mottling on the extremities, indicating poor peripheral perfusion. Auscultation of the lungs reveals crackles at the bases, suggesting pulmonary involvement potentially due to fluid overload or early acute respiratory distress syndrome (ARDS). The abdomen is mildly distended, and bowel sounds are hypoactive, raising concerns for potential ileus or early gastrointestinal involvement. Given her history of hypertension and diabetes, the patient's current hypotensive state and altered mental status are particularly alarming, suggesting a significant systemic impact.
Laboratory results return, providing further insight into the severity of the patient's condition. The white blood cell count is elevated at 18,000/mm³, with a left shift indicating a robust inflammatory response. Lactate levels are elevated at 4.5 mmol/L, confirming tissue hypoperfusion and an increased risk of organ dysfunction. Kidney function tests show elevated creatinine at 2.1 mg/dL, indicative of acute kidney injury likely due to poor perfusion and reduced urine output. Coagulation studies reveal prolonged prothrombin time (PT) and low platelet count, supporting the suspicion of disseminated intravascular coagulation (DIC) as a developing complication.
These findings necessitate prompt intervention, emphasizing fluid resuscitation and the administration of broad-spectrum antibiotics to address the underlying infection. Continuous monitoring of vital signs and organ function is crucial as the patient is at high risk for further deterioration. The initiation of vasopressors may be considered if hypotension persists despite fluid therapy. The unfolding situation demands careful clinical reasoning to prioritize interventions and anticipate the potential need for advanced organ support, such as mechanical ventilation or renal replacement therapy, as part of the evolving management plan.
Section 2
As the medical team continues to monitor the patient, a significant change in status is observed. Despite aggressive fluid resuscitation, the patient's blood pressure remains dangerously low, with readings consistently around 85/50 mmHg. Heart rate has increased to 120 beats per minute, and respiratory rate is elevated at 28 breaths per minute. Oxygen saturation has dropped to 88% on 4 liters of nasal cannula, prompting an escalation to high-flow oxygen to improve oxygenation. These changes suggest that the patient is developing septic shock, and the team must now consider the addition of vasopressors to stabilize hemodynamics.
In response to these changes, a norepinephrine infusion is initiated to address the persistent hypotension. Meanwhile, laboratory results return, revealing a further increase in lactate levels to 6.2 mmol/L, indicating worsening tissue hypoxia. The patient's mental status has deteriorated, and she is now only responsive to painful stimuli, signaling a severe systemic impact. Despite the antibiotics and supportive measures, her condition suggests the infection is not yet under control, and a review of microbiological cultures is prioritized to ensure appropriate antimicrobial coverage.
The team is also concerned about the potential progression to multi-organ dysfunction syndrome (MODS), especially given the impaired renal function and respiratory compromise. Plans are made to prepare for potential mechanical ventilation as the patient's respiratory effort becomes increasingly labored. The nursing staff is instructed to closely monitor urine output and alert the team if there is any further decline, as this might necessitate renal replacement therapy. This evolving scenario requires ongoing assessment and adjustment of the management plan based on the patient’s dynamic clinical status.
Section 3
As the team continues to manage the patient's septic shock, new diagnostic results further clarify her deteriorating condition. Repeat blood cultures reveal the presence of a resistant strain of Klebsiella pneumoniae, prompting an urgent consultation with infectious disease specialists to adjust the antibiotic regimen. The team decides to switch to a broader-spectrum antibiotic that is more likely to target the resistant organism, considering the risk of further complications from inadequately controlled infection.
In the midst of reviewing these results, an arterial blood gas (ABG) analysis returns, showing a pH of 7.25, a pCO2 of 55 mmHg, and a bicarbonate level of 18 mEq/L, indicating a mixed respiratory and metabolic acidosis. This finding underscores the severity of the patient's respiratory compromise and supports the decision to prepare for mechanical ventilation. The elevated CO2 level, paired with her increased work of breathing, suggests that her respiratory system is failing to compensate for the metabolic derangements, thus requiring further intervention to stabilize her condition.
The patient’s renal function continues to decline, with serum creatinine rising to 2.8 mg/dL and urine output dropping to less than 0.3 mL/kg/hr, raising the suspicion of acute kidney injury (AKI) secondary to septic shock. The team discusses the potential need for renal replacement therapy, such as continuous renal replacement therapy (CRRT), to manage the worsening kidney function while maintaining adequate fluid balance. This integrated approach to her care, focusing on aggressive management of both infection and organ support, remains critical as the team navigates the complexities of her evolving clinical picture.
Section 4
In the subsequent hours, the patient's condition takes a concerning turn. Her blood pressure, which had been tenuously maintained with vasopressors, begins to drop again, with readings now at 85/50 mmHg, signaling worsening hemodynamic instability. Alongside this, her heart rate escalates to 135 beats per minute, indicating compensatory tachycardia. The team quickly re-evaluates her fluid status and decides to administer an additional fluid bolus to support her circulation, while also titrating her vasopressor therapy to achieve a more stable mean arterial pressure above 65 mmHg. Concurrently, her skin becomes notably cool and mottled, with delayed capillary refill, suggesting peripheral vasoconstriction and inadequate perfusion.
New laboratory results arrive, revealing a significant drop in her platelet count to 65,000/µL, raising concerns about the potential development of disseminated intravascular coagulation (DIC), a known complication of severe sepsis. Her coagulation profile shows an elevated international normalized ratio (INR) of 1.8 and a prolonged activated partial thromboplastin time (aPTT) of 45 seconds, further supporting this suspicion. The team promptly initiates monitoring for bleeding and considers the administration of fresh frozen plasma and platelet transfusions, balancing the risks of bleeding against potential complications from transfusions.
As these developments unfold, the patient remains on mechanical ventilation with settings adjusted to optimize oxygenation and minimize further respiratory acidosis. Despite these efforts, her oxygen saturation intermittently dips below 90%, necessitating close monitoring and frequent adjustments to ventilator settings. This complex interplay of respiratory, renal, and hematological challenges requires the team to continuously integrate new information and adjust the treatment plan, ensuring that each intervention aligns with the overarching goal of stabilizing the patient and preventing further deterioration.
Section 5
As the situation progresses, the patient's renal function begins to deteriorate, indicating the development of acute kidney injury, a common complication in severe sepsis. Her urine output drops significantly, with recorded volumes of less than 20 mL/hour over the past three hours, prompting concerns about oliguria. A repeat basic metabolic panel reveals rising creatinine levels, now at 2.1 mg/dL from an earlier 1.2 mg/dL, and an elevated blood urea nitrogen (BUN) of 35 mg/dL. These findings suggest a worsening renal function, necessitating prompt intervention to prevent further renal compromise.
The clinical team responds by initiating renal replacement therapy discussions, considering the potential benefits of early dialysis to manage the patient's fluid overload and electrolyte imbalances. Meanwhile, they adjust her fluid management strategy to carefully balance hydration needs with the risk of exacerbating her kidney injury. The decision is made to continue cautious fluid resuscitation while monitoring her hemodynamic status closely, with a fluid balance chart maintained to guide further interventions.
Throughout these developments, the team remains vigilant for signs of electrolyte disturbances, such as hyperkalemia, which could pose additional threats to cardiac stability. Close monitoring of the patient's electrolyte panel reveals a potassium level of 5.6 mEq/L, prompting the administration of calcium gluconate and insulin with dextrose to stabilize the cardiac membrane potential and facilitate cellular uptake of potassium. This integrated approach underscores the importance of a multidisciplinary team in managing the complex and evolving needs of a patient with severe sepsis and its complications.