A patient with sepsis secondary to a urinary tract infection presents with metabolic acidosis and elevated lactate levels. Which nursing intervention is the highest priority to address the patient's current condition?

C) Continuing aggressive fluid resuscitation

A) Administering prescribed IV antibiotics

B) Initiating supplemental oxygen therapy

C) Continuing aggressive fluid resuscitation

D) Monitoring urine output and renal function

A patient with sepsis is demonstrating signs of worsening organ dysfunction, including declining urine output, altered mental status, and elevated liver enzymes. Despite fluid resuscitation and antibiotic therapy, blood pressure remains low. Norepinephrine is initiated to stabilize hemodynamics. Which nursing intervention is a priority to assess the effectiveness of the current treatment plan?

B) Evaluate the patient's urine output hourly.

A) Monitor the patient's peripheral pulses.

B) Evaluate the patient's urine output hourly.

C) Reassess the patient's skin turgor.

D) Check the patient's capillary refill time.

A patient with sepsis is receiving norepinephrine to maintain adequate blood pressure and organ perfusion. The nurse notices a decrease in urine output to 15 mL/hour, an increase in serum creatinine levels, and altered mental status. Which nursing intervention is the most appropriate to address the potential complications of multiple organ dysfunction syndrome (MODS) in this patient?

C) Notify the healthcare provider for possible adjustment of vasopressor therapy.

A) Increase the rate of norepinephrine infusion to improve blood pressure.

B) Administer a bolus of intravenous fluids to improve kidney perfusion.

C) Notify the healthcare provider for possible adjustment of vasopressor therapy.

D) Increase the frequency of neurological assessments to monitor for changes in mental status.

A patient with suspected acute respiratory distress syndrome (ARDS) is experiencing respiratory acidosis and hypoxemia, despite receiving high-flow nasal cannula oxygen therapy. What is the most appropriate initial nursing intervention to optimize the patient's oxygenation and ventilation?

C) Position the patient in prone position

A) Increase the oxygen flow rate to 100%

B) Prepare the patient for endotracheal intubation and mechanical ventilation

C) Position the patient in prone position

D) Administer a bronchodilator to improve airflow

A patient with suspected ARDS is experiencing respiratory acidosis and hypoxemia despite high-flow nasal cannula. Which nursing intervention is most appropriate to address the patient's respiratory status and prevent further complications?

B) Prepare the patient for intubation and mechanical ventilation.

A) Increase the flow rate on the nasal cannula to deliver more oxygen.

B) Prepare the patient for intubation and mechanical ventilation.

C) Position the patient in semi-Fowler's to facilitate lung expansion.

D) Administer a bronchodilator to alleviate respiratory distress.

A patient with acute respiratory distress syndrome (ARDS) is on mechanical ventilation with low tidal volumes and higher PEEP. Despite these measures, the patient continues to exhibit respiratory acidosis and refractory hypoxemia, with arterial blood gases showing a pH of 7.28, PaCO2 of 60 mmHg, and PaO2 of 60 mmHg. Which of the following interventions should the nurse anticipate next to optimize the patient's oxygenation and ventilation?

B) Initiate prone positioning therapy

A) Increase the tidal volume to improve ventilation

B) Initiate prone positioning therapy

C) Administer a bolus of intravenous fluids

D) Reduce the PEEP to decrease barotrauma risk

A patient on mechanical ventilation is experiencing respiratory acidosis and refractory hypoxemia, with arterial blood gases showing a pH of 7.28, PaCO2 of 60 mmHg, and PaO2 of 60 mmHg. The nephrology team has recommended continuous renal replacement therapy (CRRT) due to acute kidney injury and hemodynamic instability. Which of the following nursing interventions is most critical at this time to support the patient's respiratory and renal function?

C) Implement strict monitoring of fluid input and output to optimize CRRT effectiveness.

A) Increase the tidal volume on the ventilator to improve oxygenation.

B) Administer a diuretic to increase urine output and reduce fluid overload.

C) Implement strict monitoring of fluid input and output to optimize CRRT effectiveness.

D) Decrease the PEEP to reduce the risk of barotrauma.

A patient in the ICU is experiencing hemodynamic instability with a MAP of 55 mmHg, tachycardia, low CVP, minimal urine output, and elevated lactate levels. The patient is receiving norepinephrine and vasopressin. Which nursing intervention is the priority to address the patient's condition?

C) Monitor cardiac output and adjust vasopressor support based on hemodynamic parameters.

A) Increase the rate of IV fluid administration to improve intravascular volume.

B) Initiate continuous renal replacement therapy to manage oliguria and correct fluid balance.

C) Monitor cardiac output and adjust vasopressor support based on hemodynamic parameters.

D) Administer a diuretic to reduce potential fluid overload and improve cardiac function.

A patient in the intensive care unit is experiencing hemodynamic instability and hypoxia despite aggressive management with fluids and vasopressors. The bedside echocardiogram shows a moderately reduced left ventricular ejection fraction of 40%. Which nursing intervention is most appropriate to prioritize at this time to address the patient's condition?

B) Collaborate with the respiratory therapist to optimize ventilator settings to improve oxygenation.

A) Increase the rate of intravenous fluid administration to improve preload.

B) Collaborate with the respiratory therapist to optimize ventilator settings to improve oxygenation.

C) Prepare for the immediate administration of a diuretic to reduce cardiac workload.

D) Suggest the addition of a beta-blocker to improve cardiac function.

sepsis - Nursing Case Study

Pathophysiology

• Primary mechanism: Sepsis begins with an overwhelming immune response to infection, where the release of pro-inflammatory cytokines causes widespread inflammation, leading to endothelial damage and increased vascular permeability.

• Secondary mechanism: This systemic inflammation results in the dysregulation of coagulation pathways, causing disseminated intravascular coagulation (DIC), which further exacerbates tissue hypoperfusion and organ dysfunction.

• Key complication: The combination of hypotension, impaired oxygen delivery, and microvascular thrombosis contributes to multi-organ failure, a critical concern in sepsis management.

Patient Profile

Demographics:

65-year-old male, retired teacher

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Previous myocardial infarction

• Current medications: Lisinopril, Metformin, Aspirin, Atorvastatin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Fever and confusion

• Key symptoms: High fever, chills, increased heart rate, difficulty breathing, decreased urine output, altered mental status

• Vital signs: Temperature 39.5°C (103.1°F), Heart rate 120 bpm, Respiratory rate 28 breaths per minute, Blood pressure 90/60 mmHg, Oxygen saturation 90% on room air

Section 1

New Diagnostic Results:

As the healthcare team continues to monitor the patient's condition, additional diagnostic tests are conducted to further assess the severity of the sepsis and identify the underlying source of infection. Blood cultures reveal the presence of gram-negative bacteria, suggesting a possible urinary tract infection as the primary source. Urinalysis shows elevated levels of white blood cells and the presence of nitrites, confirming a urinary infection. Furthermore, a complete blood count indicates leukocytosis with a white blood cell count of 18,000/mm³, signaling an active inflammatory response.

In addition to these findings, arterial blood gas analysis presents a concerning picture: the patient exhibits metabolic acidosis with a pH of 7.28, bicarbonate level of 18 mmol/L, and elevated lactate level of 4.5 mmol/L, indicative of tissue hypoperfusion and anaerobic metabolism. These results underscore the urgency of reversing the hypoperfusion and addressing the infection to prevent further deterioration.

These diagnostic results necessitate a prompt escalation of care. The medical team initiates broad-spectrum intravenous antibiotics tailored to cover gram-negative organisms while awaiting sensitivity results. Concurrently, aggressive fluid resuscitation is continued to stabilize blood pressure and improve organ perfusion. The patient's response to these interventions will be closely monitored, with particular attention to changes in vital signs, urine output, and mental status, as these will provide crucial information on the effectiveness of the treatment strategy and guide further adjustments.

Section 2

As the treatment progresses, the healthcare team observes a change in the patient's status that prompts further evaluation. Despite ongoing fluid resuscitation and antibiotic therapy, the patient's blood pressure remains borderline at 88/54 mmHg, and there is a concerning trend of decreasing urine output, now at 20 mL/hour. The patient's heart rate remains elevated at 112 beats per minute, and they exhibit increased respiratory effort with a rate of 24 breaths per minute. Mental status is somewhat altered; the patient is less alert and only intermittently oriented to time and place.

New diagnostic results indicate that the patient's serum creatinine level has risen to 2.1 mg/dL from a baseline of 0.9 mg/dL, suggesting acute kidney injury possibly related to persistent hypoperfusion. Additionally, liver function tests reveal elevated transaminases, with AST at 85 U/L and ALT at 98 U/L, raising concerns about potential hepatic involvement. These findings suggest a progression towards multiple organ dysfunction syndrome (MODS), necessitating an urgent reassessment of the current treatment strategy.

Given these developments, the medical team considers the need for vasopressor support to maintain adequate blood pressure and organ perfusion. Norepinephrine is initiated to stabilize hemodynamics while continuing to optimize fluid management. The focus now shifts to closely monitoring the patient's response to these escalated interventions, with an emphasis on tracking changes in urine output, mental status, and laboratory markers of organ function. The evolving clinical picture requires diligent teamwork and communication to adjust the care plan and anticipate further complications in this complex case of sepsis.

Section 3

As the medical team continues to monitor the patient's condition, a new complication arises that demands urgent attention. Despite the initiation of norepinephrine to support blood pressure, the patient develops signs of respiratory distress, suggesting potential progression to acute respiratory distress syndrome (ARDS). The patient's oxygen saturation, previously stable, drops to 88% on high-flow nasal cannula delivering 60% oxygen. Auscultation of the lungs reveals diffuse crackles, indicating fluid accumulation and impaired gas exchange. A chest X-ray is promptly ordered and reveals bilateral pulmonary infiltrates, consistent with ARDS.

Simultaneously, the patient's neurological status further deteriorates. The patient becomes lethargic and minimally responsive to verbal stimuli, with a Glasgow Coma Scale (GCS) score now at 10. This decline in mental status, coupled with the elevated creatinine and liver enzyme levels, underscores the gravity of the situation and the potential for worsening multiple organ dysfunction. Arterial blood gas analysis shows a pH of 7.32, PaCO2 of 58 mmHg, and PaO2 of 55 mmHg, indicating respiratory acidosis with hypoxemia, further complicating the clinical picture.

In response to these developments, the healthcare team considers escalating respiratory support and contemplates the need for mechanical ventilation to optimize oxygenation and ventilation. The intensivist discusses the possibility of implementing lung-protective ventilation strategies to mitigate the risk of ventilator-induced lung injury. Concurrently, nephrology and hepatology consultations are requested to address the acute kidney injury and hepatic dysfunction. The team remains vigilant, recognizing the need for continuous reassessment and adjustment of the treatment plan to manage the evolving complications in this critically ill patient.

Section 4

The medical team decides to proceed with mechanical ventilation to address the patient's worsening respiratory status. After intubation, the patient is placed on a lung-protective ventilation strategy with low tidal volumes and higher PEEP to improve oxygenation while minimizing the risk of further lung injury. Despite these efforts, the patient's oxygen saturation remains tenuous, fluctuating between 85% and 90%. The team carefully monitors arterial blood gases, which show a pH of 7.28, PaCO2 of 60 mmHg, and PaO2 of 60 mmHg, indicating persistent respiratory acidosis and refractory hypoxemia.

In parallel, the nephrology team evaluates the patient's renal function in light of rising creatinine levels, which have now reached 3.2 mg/dL, suggesting worsening acute kidney injury. Urine output has decreased significantly to less than 0.3 mL/kg/hr over the past six hours. Given the patient's hemodynamic instability and deteriorating renal function, the nephrologist recommends initiating continuous renal replacement therapy (CRRT) to manage fluid overload and support renal function without further compromising blood pressure.

As the team implements these interventions, they remain vigilant for signs of further complications. The intensivist emphasizes the importance of a multidisciplinary approach, coordinating with nephrology, hepatology, and respiratory therapy to reassess the patient's status continually. This ongoing collaboration ensures that any subtle changes in clinical parameters are promptly addressed, with a focus on optimizing organ support and preventing further deterioration. The patient's condition remains critical, and the team prepares for potential interventions to address any new developments.

Section 5

As the critical care team continues to monitor the patient's condition closely, a significant change in the patient's status is observed. Over the next several hours, the patient's hemodynamics become increasingly unstable, with the mean arterial pressure (MAP) dropping to 55 mmHg despite aggressive fluid resuscitation and vasopressor support. The intensivist notes that the patient's heart rate has increased to 125 beats per minute, and the central venous pressure (CVP) remains low at 4 mmHg, indicating persistent hypovolemia and possible septic shock progression. Concurrently, the patient's urinary output remains minimal, further complicating the management of fluid balance and renal perfusion.

In response to the patient's declining status, the team decides to adjust the vasopressor regimen, increasing the dosage of norepinephrine and adding vasopressin to improve vascular tone and support blood pressure. The decision is made to perform a bedside echocardiogram to assess cardiac function and exclude the development of new cardiac complications such as cardiomyopathy or pericardial effusion, which could contribute to the patient's hemodynamic instability. The echocardiogram reveals moderately reduced left ventricular ejection fraction (LVEF) at 40%, suggesting sepsis-related cardiac dysfunction as a contributing factor.

Despite these interventions, the patient's oxygenation metrics remain inadequate, with SpO2 persistently struggling to rise above 88%. The respiratory therapy team collaborates to fine-tune ventilator settings, reassessing the balance of PEEP and tidal volume to optimize gas exchange while minimizing barotrauma risk. Meanwhile, laboratory results indicate an elevated lactate level of 5.5 mmol/L, reinforcing concerns about tissue hypoxia and metabolic acidosis. The team recognizes the need for a dynamic, integrative approach, emphasizing the importance of reevaluating all organ systems continually to anticipate and mitigate emerging complications in this complex, rapidly evolving clinical scenario.