A patient with severe burns is exhibiting signs of respiratory distress and oliguria 24 hours post-injury. Which of the following is the most appropriate initial nursing intervention to address the patient's respiratory status?

C) Elevate the head of the bed and apply continuous positive airway pressure (CPAP).

A) Increase the rate of the intravenous fluid infusion to improve circulation.

B) Administer a diuretic to reduce fluid overload and improve respiratory function.

C) Elevate the head of the bed and apply continuous positive airway pressure (CPAP).

D) Perform chest physiotherapy to mobilize secretions and improve lung expansion.

A patient with full thickness burns is exhibiting signs of respiratory distress and oliguria. The nurse notes diminished breath sounds, crackles, and a respiratory rate of 32 breaths per minute with an oxygen saturation of 88% despite supplemental oxygen. Urine output is less than 20 mL/hour, and laboratory tests show elevated BUN and creatinine levels. What is the nurse's priority intervention?

D) Call the healthcare provider to discuss the need for intubation and mechanical ventilation

A) Increase the rate of IV fluid administration to improve renal perfusion

B) Administer a diuretic to reduce pulmonary edema

C) Initiate high-flow oxygen therapy to improve oxygenation

D) Call the healthcare provider to discuss the need for intubation and mechanical ventilation

A patient with acute respiratory distress syndrome (ARDS) and suspected sepsis is receiving non-invasive positive pressure ventilation (NIPPV) and broad-spectrum antibiotics. The nurse observes an increase in the patient's respiratory rate and a decrease in oxygen saturation. Which intervention should the nurse prioritize?

C) Prepare for intubation and mechanical ventilation.

A) Increase the FiO2 on the NIPPV device.

B) Administer a diuretic to reduce pulmonary edema.

C) Prepare for intubation and mechanical ventilation.

D) Increase the rate of IV fluid administration.

A patient with acute respiratory distress syndrome (ARDS) and acute kidney injury (AKI) presents with increased respiratory distress and elevated serum lactate levels. Which nursing intervention should be prioritized to address the potential complications associated with these findings?

D) Adjust the settings on non-invasive positive pressure ventilation to optimize oxygenation.

A) Increase fluid administration to improve tissue perfusion.

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

C) Administer diuretics to reduce pulmonary edema.

D) Adjust the settings on non-invasive positive pressure ventilation to optimize oxygenation.

A patient with worsening respiratory acidosis and signs of sepsis is being prepared for invasive mechanical ventilation. Which nursing intervention is most critical to prioritize before intubation to enhance patient outcomes?

B) Initiating norepinephrine infusion to improve systemic perfusion

A) Administering a bolus of IV fluids to address hypotension

B) Initiating norepinephrine infusion to improve systemic perfusion

C) Providing sedation and analgesia to ensure patient comfort

D) Reevaluating the effectiveness of empirical antibiotics before intubation

A patient with sepsis and acute kidney injury is being prepared for invasive mechanical ventilation due to worsening respiratory acidosis. Which nursing intervention is most critical to perform before initiating mechanical ventilation?

C) Verify the correct endotracheal tube size and equipment for intubation.

A) Administer the full dose of norepinephrine to address hypotension.

B) Ensure that the patient's electrolyte levels are within normal limits.

C) Verify the correct endotracheal tube size and equipment for intubation.

D) Reassess the patient's pain level and administer analgesics as needed.

A patient with sepsis is showing signs of worsening renal perfusion, hyperkalemia, and fluctuating blood pressure despite norepinephrine infusion. As a nurse, what is the priority intervention to address the patient's current condition?

C) Prepare for continuous renal replacement therapy (CRRT)

A) Increase the dose of norepinephrine to improve blood pressure

B) Administer calcium gluconate to address hypocalcemia

C) Prepare for continuous renal replacement therapy (CRRT)

D) Administer a bolus of normal saline to increase urine output

A patient with sepsis on norepinephrine infusion and invasive mechanical ventilation has developed oliguria, hyperkalemia, and hypotension, with lactate levels of 4.5 mmol/L. The healthcare team is considering initiating continuous renal replacement therapy (CRRT). What is the primary rationale for initiating CRRT in this clinical scenario?

D) To prevent further organ damage by managing electrolyte imbalances

A) To correct metabolic acidosis and remove excess lactate

B) To provide adequate nutrition and electrolyte replacement

C) To maintain hemodynamic stability by removing fluid overload

D) To prevent further organ damage by managing electrolyte imbalances

A patient undergoing continuous renal replacement therapy (CRRT) has a serum potassium level of 5.5 mEq/L and a lactic acidosis with a lactate level of 4.8 mmol/L. Despite norepinephrine infusion, the systolic blood pressure fluctuates between 85 and 92 mmHg. Which nursing intervention is most appropriate in this situation?

C) Collaborate with the healthcare team to initiate another vasopressor to improve blood pressure.

A) Increase the norepinephrine infusion rate to maintain a stable blood pressure.

B) Prepare to administer calcium gluconate to stabilize cardiac membranes.

C) Collaborate with the healthcare team to initiate another vasopressor to improve blood pressure.

D) Recommend stopping CRRT to prevent further electrolyte imbalances.

A patient receiving continuous renal replacement therapy (CRRT) exhibits fluctuating systolic blood pressure between 85 and 92 mmHg, despite increased norepinephrine infusion. Their skin is cool and mottled, and arterial blood gas analysis shows lactic acidosis with a lactate level of 4.8 mmol/L. Which nursing intervention is the most appropriate to address the patient's hemodynamic instability?

B) Collaborate with the healthcare team to initiate additional vasopressor or inotropic support.

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

B) Collaborate with the healthcare team to initiate additional vasopressor or inotropic support.

C) Administer a bolus of normal saline to improve tissue perfusion.

D) Reduce the CRRT flow rate to allow for more gradual fluid removal.

Full Thickness Burns - Nursing Case Study

Pathophysiology

• Primary mechanism: Full thickness burns destroy the epidermis, dermis, and potentially subcutaneous tissues, leading to the loss of skin's protective barrier, which exposes underlying tissues to infection and fluid loss.

• Secondary mechanism: Thermal injury induces coagulation necrosis, resulting in the denaturation of proteins within the affected area. This impairs cellular function and halts normal metabolic processes, leading to tissue death and eschar formation.

• Key complication: The destruction of dermal structures, including nerves and blood vessels, leads to significant loss of sensation and compromised blood flow, increasing the risk of tissue ischemia and necrosis, which can complicate healing and increase the risk of systemic infection (sepsis).

Patient Profile

Demographics:

45-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Lisinopril, Metformin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe burns sustained from a workplace accident

• Key symptoms: Large areas of skin charring, intense pain, difficulty breathing, reduced urine output

• Vital signs: Temperature 101.5°F, Heart rate 122 bpm, Blood pressure 100/60 mmHg, Respiratory rate 28 breaths per minute, Oxygen saturation 92% on room air

Section 1

New Complications

As the patient progresses through the initial treatment phase, he begins to exhibit signs of potential complications. Over the course of the next 24 hours, his respiratory status deteriorates, prompting additional assessments. The patient develops increased respiratory distress, evidenced by a further increase in respiratory rate to 32 breaths per minute and a drop in oxygen saturation to 88% even with supplemental oxygen. Auscultation reveals diminished breath sounds, particularly in the lower lobes, and the presence of crackles, suggesting a potential development of pulmonary edema or acute respiratory distress syndrome (ARDS) as a complication of systemic inflammatory response and fluid resuscitation.

In conjunction with respiratory decline, the patient’s urine output remains critically low, measuring less than 20 mL/hour, despite aggressive fluid management. This oliguria raises concerns about acute kidney injury (AKI), likely secondary to hypoperfusion and the systemic effects of the burn injury. Laboratory tests reveal elevated blood urea nitrogen (BUN) and creatinine levels, confirming the suspicion of renal impairment. Additionally, the patient’s white blood cell count is markedly elevated, suggesting an inflammatory or infectious process that could be indicative of early sepsis. The presence of these complications necessitates a reevaluation of the current management plan, including potential adjustments in fluid therapy, initiation of antibiotics, and reassessment of the need for advanced respiratory support.

These developments require the healthcare team to engage in critical clinical reasoning to prioritize interventions that address the evolving respiratory and renal challenges while mitigating the risk of infection. The patient’s condition underscores the complexity of managing full thickness burns and emphasizes the need for vigilant monitoring and timely intervention to prevent further deterioration. The team must anticipate the potential for additional complications, such as systemic infection, and be prepared to escalate care as necessary to stabilize the patient's condition.

Section 2

As the healthcare team responds to the patient's deteriorating condition, they prioritize further diagnostic evaluations to better understand the underlying causes of the new complications. A chest X-ray is promptly ordered, revealing bilateral infiltrates consistent with pulmonary edema, supporting the suspicion of acute respiratory distress syndrome (ARDS). This finding aligns with the patient's clinical presentation of increased respiratory distress and hypoxemia. To address the respiratory compromise, the team initiates non-invasive positive pressure ventilation (NIPPV) to improve oxygenation and reduce the work of breathing. Continuous monitoring of arterial blood gases is implemented to assess the effectiveness of this intervention and guide further respiratory management.

In parallel, a comprehensive laboratory panel is conducted to evaluate the patient’s renal function and assess for potential sepsis, given the elevated white blood cell count observed earlier. Repeat blood tests show a further increase in BUN and creatinine levels, confirming progression of acute kidney injury (AKI). Additionally, serum lactate levels are elevated, raising concerns about tissue hypoperfusion and sepsis. Blood cultures are obtained to identify any infectious organisms, and broad-spectrum antibiotics are initiated empirically to address the potential septic process while awaiting culture results.

Despite these interventions, the patient's condition remains precarious. The team must now consider the balance between adequate fluid resuscitation to support organ perfusion and the risk of exacerbating pulmonary edema. This necessitates careful titration of fluids and possible initiation of renal replacement therapy if kidney function continues to decline. The situation highlights the importance of dynamic clinical reasoning and adaptability in managing the complex interplay of respiratory and renal complications in burn patients. The team remains vigilant for further complications and is prepared to modify the treatment plan as the patient's response to interventions unfolds.

Section 3

Following the initiation of non-invasive positive pressure ventilation (NIPPV) and empirical antibiotics, the healthcare team closely monitors the patient's response to these interventions. Despite initial stabilization, the patient's respiratory status begins to deteriorate overnight. Vital signs reveal a persistent tachycardia with a heart rate of 118 beats per minute, hypotension at 88/54 mmHg, and a fever of 38.5°C (101.3°F). Oxygen saturation remains suboptimal at 88% on NIPPV, and the patient exhibits increased work of breathing with accessory muscle use and nasal flaring.

Repeat arterial blood gas analysis shows a worsening respiratory acidosis, with pH 7.28, PaCO2 52 mmHg, and PaO2 60 mmHg. The clinical team recognizes that the current mode of ventilation is insufficient to maintain adequate gas exchange and decides to escalate to invasive mechanical ventilation to provide more controlled respiratory support. Concurrently, the decision is made to initiate a low-dose vasopressor, norepinephrine, to address the hypotension and improve systemic perfusion.

As the patient is prepared for intubation, the team reviews the latest laboratory results and notes a further elevation in serum creatinine to 3.2 mg/dL and BUN to 58 mg/dL, indicating worsening acute kidney injury. Blood cultures return positive for gram-negative rods, confirming a septic process likely linked to the wound infection. The team adjusts the antibiotic regimen based on sensitivity results to target the specific organism more effectively. With these developments, the focus shifts to maintaining hemodynamic stability and preventing further organ dysfunction, while the multidisciplinary team remains alert for additional complications such as electrolyte imbalances and potential for multi-organ failure.

Section 4

Following the initiation of invasive mechanical ventilation and norepinephrine infusion, the team's focus shifts to stabilizing the patient and monitoring for further complications. Despite these interventions, the patient's condition exhibits concerning changes. Early in the morning, the nursing staff notices a decline in urine output, now at 10 mL over the past two hours, signaling worsening renal perfusion. Further lab results reveal hyperkalemia, with serum potassium rising to 5.8 mEq/L, and a drop in ionized calcium levels to 1.0 mmol/L, suggesting an imbalance likely exacerbated by the ongoing acute kidney injury and the body's stress response to sepsis.

The patient's skin, previously warm and flushed, now feels cooler and mottled, particularly on the extremities, indicating potential progression towards distributive shock. Despite the norepinephrine infusion, blood pressure remains labile, with systolic readings fluctuating between 82 and 90 mmHg. Lactate levels have increased to 4.5 mmol/L, further confirming inadequate tissue perfusion and oxygenation. The healthcare team recognizes the need for swift intervention to prevent further deterioration, considering options such as increasing vasopressor support, optimizing fluid management, and addressing the electrolyte disturbances.

In a collaborative effort, the multidisciplinary team, including nephrology and critical care specialists, convenes to reassess the treatment strategy. The decision is made to initiate continuous renal replacement therapy (CRRT) to address the acute kidney injury and manage the electrolyte imbalances. Meanwhile, critical care nurses focus on ensuring meticulous monitoring of hemodynamic parameters and early detection of any signs of multi-organ failure. The team remains vigilant, understanding the delicate balance required to stabilize the patient's condition while preventing additional complications.

Section 5

The initiation of continuous renal replacement therapy (CRRT) begins to yield some positive changes in the patient's clinical status. Within the first few hours, there is a slight improvement in urine output, now recorded at 30 mL over two hours. The nephrology team closely monitors these changes, adjusting dialysis parameters to optimize fluid removal and electrolyte balance. Despite this progress, serum potassium levels remain elevated at 5.5 mEq/L, necessitating ongoing vigilance and potential adjustments in therapy. Ionized calcium levels have stabilized at 1.1 mmol/L, reflecting a modest correction in electrolyte disturbances.

However, the patient's hemodynamic status remains precarious. The nursing staff observes that despite the increased norepinephrine infusion, the systolic blood pressure continues to fluctuate, now ranging between 85 and 92 mmHg. The patient's skin remains cool and mottled, and there is an emerging concern about the possibility of worsening distributive shock and the risk of developing multi-organ dysfunction. Arterial blood gas analysis reveals a persistent lactic acidosis with a lactate level of 4.8 mmol/L, underscoring the need for improved tissue perfusion and oxygenation.

In response to these challenges, the critical care team considers the potential need for additional vasopressors or inotropic support to stabilize blood pressure and enhance cardiac output. They also deliberate on the possibility of further fluid resuscitation, weighing the risks of fluid overload against the necessity for adequate perfusion. As the team refines their treatment plan, they remain acutely aware of the patient's fragile state, prioritizing interventions that could avert the progression to multi-organ failure and promote recovery from the acute crisis.