A patient presents with third-degree burns covering 45% of his TBSA, showing signs of respiratory distress and shock. Despite initiation of fluid resuscitation and oxygen therapy, which intervention should the nurse prioritize to address the patient's respiratory acidosis and hypoxemia?

D) Assist with endotracheal intubation and mechanical ventilation to secure the airway.

A) Continue monitoring vital signs and administer analgesics for pain management.

B) Prepare for emergency escharotomy to improve ventilation and perfusion.

C) Administer sodium bicarbonate to correct metabolic acidosis.

D) Assist with endotracheal intubation and mechanical ventilation to secure the airway.

A patient with extensive third-degree burns over 45% of the total body surface area presents with signs of respiratory distress. Following initial interventions including high-flow oxygen therapy and fluid resuscitation, the patient exhibits worsening hypoxemia and increased work of breathing. What is the most appropriate next step in managing this patient's condition?

C) Perform endotracheal intubation and mechanical ventilation to secure the airway and manage respiratory failure.

A) Initiate non-invasive ventilation to improve oxygenation and reduce work of breathing.

B) Administer a bronchodilator to address wheezing and improve airway patency.

C) Perform endotracheal intubation and mechanical ventilation to secure the airway and manage respiratory failure.

D) Increase fluid resuscitation rate to address potential hypoperfusion and improve oxygen delivery.

A patient with significant thermal injuries and suspected inhalation injury is exhibiting deteriorating respiratory function, hemodynamic instability, hyperkalemia, and reduced urine output. As the nurse, which of the following interventions should be prioritized to address the immediate life-threatening complication?

C) Prepare for rapid sequence intubation to secure the airway and improve oxygenation.

A) Administer calcium gluconate to stabilize the cardiac membrane and combat hyperkalemia effects.

B) Initiate continuous renal replacement therapy to manage acute kidney injury and fluid overload.

C) Prepare for rapid sequence intubation to secure the airway and improve oxygenation.

D) Increase intravenous fluid resuscitation to counteract hypotension and support circulation.

A patient with a thermal injury and inhalation damage is exhibiting signs of deteriorating respiratory function, hypotension, and oliguria. Despite aggressive fluid resuscitation, the hypotension persists, and there is evidence of acute kidney injury. What is the most appropriate nursing intervention to prioritize at this time?

C) Assist with the intubation process to secure the airway.

A) Increase the rate of fluid resuscitation to address hypotension.

B) Prepare for immediate dialysis to manage hyperkalemia and oliguria.

C) Assist with the intubation process to secure the airway.

D) Administer an additional dose of broad-spectrum antibiotics.

A 54-year-old patient with a history of inhalation injury and systemic inflammatory response is showing signs of acute respiratory distress syndrome (ARDS) and refractory septic shock, despite current treatment. As the critical care nurse, what is the most appropriate next step in managing the patient's complex condition?

B) Initiate continuous renal replacement therapy (CRRT) to address electrolyte imbalances and fluid overload.

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

B) Initiate continuous renal replacement therapy (CRRT) to address electrolyte imbalances and fluid overload.

C) Administer a fluid bolus to improve hemodynamic stability.

D) Decrease the positive end-expiratory pressure (PEEP) to reduce barotrauma risk.

A patient with a recent diagnosis of ARDS secondary to inhalation injury is experiencing refractory septic shock and worsening renal function. Despite the use of norepinephrine, the mean arterial pressure is persistently low, and lactate levels are elevated. The healthcare team is considering adjunctive therapies. Which of the following interventions should the nurse anticipate implementing to best address the patient's current clinical status and prevent further deterioration?

C) Administer corticosteroids to reduce systemic inflammation.

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

B) Initiate dopamine infusion to augment cardiac output.

C) Administer corticosteroids to reduce systemic inflammation.

D) Discontinue norepinephrine and start high-dose vasopressin.

A 68-year-old patient in the ICU shows signs of neurological deterioration with a Glasgow Coma Scale (GCS) score of 6 and anisocoria, alongside laboratory findings indicating metabolic acidosis and a high anion gap. Which nursing intervention is the most critical to perform first to address the potential neurological risks associated with increased intracranial pressure (ICP) and metabolic acidosis?

D) Adjust the ventilator settings to ensure adequate oxygenation and CO2 removal.

A) Administer mannitol as prescribed to reduce cerebral edema.

B) Prepare the patient for immediate insertion of an ICP monitor.

C) Initiate continuous renal replacement therapy (CRRT) to correct acid-base imbalance.

D) Adjust the ventilator settings to ensure adequate oxygenation and CO2 removal.

A patient with a deteriorating neurological status is being assessed by the nursing team. The patient has a Glasgow Coma Scale (GCS) score of 6, anisocoria, and metabolic acidosis with a pH of 7.22. Which of the following interventions should the nurse prioritize to address the suspected increased intracranial pressure (ICP) while considering the patient's overall critical condition?

C) Elevate the head of the bed to 30 degrees to facilitate venous drainage.

A) Administer a hypertonic saline bolus to reduce cerebral edema.

B) Increase the ventilator rate to induce mild hyperventilation and decrease cerebral blood flow.

C) Elevate the head of the bed to 30 degrees to facilitate venous drainage.

D) Administer sodium bicarbonate to correct metabolic acidosis.

A patient in the ICU with diffuse cerebral edema and worsening respiratory acidosis is receiving hypertonic saline and CRRT. Despite interventions, the patient remains hemodynamically unstable. As the nurse, what is the priority action to support the patient's neurological and overall status?

A) Increase the rate of norepinephrine infusion to maintain cerebral perfusion pressure.

B) Administer a diuretic to rapidly reduce cerebral edema.

C) Adjust the ventilator settings to increase oxygenation and reduce PaCO2.

D) Perform passive range of motion exercises to prevent muscle atrophy.

A patient in critical care is experiencing increased intracranial pressure (ICP) and worsening respiratory acidosis, despite adjustments to ventilator settings and administration of hypertonic saline. Continuous renal replacement therapy (CRRT) has been initiated. The patient remains hemodynamically unstable. As the nurse, what is the most critical action to prioritize in this situation to stabilize the patient?

C) Re-evaluate and adjust ventilator settings to improve gas exchange and reduce acidosis.

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

B) Initiate sedation to reduce metabolic demand and control the patient's agitation.

C) Re-evaluate and adjust ventilator settings to improve gas exchange and reduce acidosis.

D) Administer additional diuretics to further reduce cerebral edema and manage fluid balance.

burns - Nursing Case Study

Pathophysiology

• Primary mechanism: Thermal injury leads to direct cellular damage and protein denaturation, causing necrosis and initiating inflammatory responses. This disrupts skin integrity, resulting in fluid loss and increased risk of infection.

• Secondary mechanism: The inflammatory cascade triggers systemic vasodilation and increased capillary permeability, leading to significant plasma leakage, hypovolemia, and potential shock. This systemic response can compromise organ perfusion, exacerbating injury.

• Key complication: Severe burns can progress to systemic inflammatory response syndrome (SIRS) and multi-organ dysfunction syndrome (MODS), where widespread inflammation impairs organ function, significantly increasing mortality risk.

Patient Profile

Demographics:

42-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes, Smoking history

• Current medications: Lisinopril, Metformin, Insulin, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Extensive third-degree burns from an industrial accident

• Key symptoms: Severe pain, difficulty breathing, decreased urine output

• Vital signs: Blood pressure 90/50 mmHg, Heart rate 130 bpm, Respiratory rate 32 breaths/min, Temperature 39.2°C (102.6°F), Oxygen saturation 85% on room air

Section 1

Initial assessment findings reveal the critical condition of the patient upon arrival at the emergency department. The patient is found to have extensive third-degree burns covering approximately 45% of his total body surface area (TBSA), predominantly affecting the torso, upper arms, and face. The burn wounds appear leathery and charred, indicative of full-thickness injury. Immediate concern arises from the inhalation injury, suggested by the presence of soot around the nares and in the oropharynx, coupled with his labored breathing. Auscultation of the lungs reveals diminished breath sounds bilaterally with faint wheezing, indicating potential airway compromise and necessitating rapid intervention. The patient's vital signs reflect a state of shock, with hypotension, tachycardia, and tachypnea, alongside hyperthermia and hypoxemia, raising suspicion for acute respiratory distress syndrome (ARDS) secondary to the burn injury and systemic inflammatory response.

Laboratory results further compound concerns, revealing a markedly elevated white blood cell count of 22,000/mm³, suggesting a robust inflammatory response or potential early onset infection. Arterial blood gas analysis indicates a pH of 7.25, PaCO2 of 50 mmHg, and PaO2 of 60 mmHg, confirming respiratory acidosis with hypoxemia, consistent with impending respiratory failure. Renal function tests show a serum creatinine of 2.5 mg/dL and an elevated blood urea nitrogen of 35 mg/dL, signaling acute kidney injury likely due to hypoperfusion and potential rhabdomyolysis from muscle damage. Electrolyte imbalances are evident, with a sodium level of 130 mEq/L and potassium level of 6.0 mEq/L, necessitating immediate correction to prevent cardiac complications.

In response to these findings, aggressive fluid resuscitation is initiated using the Parkland formula, targeting the replenishment of intravascular volume to stabilize hemodynamics. High-flow oxygen therapy is commenced, and preparations for possible intubation are made to secure the airway and improve oxygenation. The multidisciplinary team prepares for escharotomy procedures to relieve compartment syndrome from circumferential burns. Despite these interventions, the patient's condition remains precarious, with ongoing risk for further complications such as sepsis or MODS. The team must employ advanced clinical reasoning to continuously reassess and adapt the treatment plan, closely monitoring for signs of deterioration or new complications along this complex and challenging clinical trajectory.

Section 2

As the medical team continues to manage the patient, a sudden change in status prompts immediate attention. Despite initial stabilization efforts, the patient exhibits signs of deteriorating respiratory function, with increasing difficulty in maintaining adequate oxygenation. Repeat arterial blood gas analysis reveals a worsening respiratory acidosis, with a pH now at 7.20, PaCO2 rising to 55 mmHg, and PaO2 dropping to 55 mmHg. The diminished breath sounds and wheezing have progressed to audible stridor, indicating significant upper airway obstruction likely exacerbated by ongoing edema from thermal injury and inhalation damage. The decision is made to proceed with intubation to secure the airway, as the risk of complete obstruction becomes imminent.

Concurrently, the patient's hemodynamic status remains unstable. Despite aggressive fluid resuscitation, he exhibits persistent hypotension with a blood pressure of 85/50 mmHg and a heart rate that has climbed to 130 beats per minute. This hypotensive state, resistant to fluid therapy, suggests a potential transition from hypovolemic to distributive shock, possibly due to evolving sepsis. Blood cultures are drawn, and broad-spectrum antibiotics are promptly initiated to preemptively address this risk. Meanwhile, the electrolyte imbalance persists despite corrective measures, with the potassium level stubbornly high at 6.2 mEq/L, necessitating continuous cardiac monitoring and further intervention to prevent arrhythmias.

The evolving picture of acute kidney injury also becomes more concerning, as urine output diminishes significantly, dropping to less than 20 mL/hour, indicative of oliguria. Repeat renal function tests show a creatinine level rising to 3.0 mg/dL, reinforcing the need for renal protective strategies and possibly renal replacement therapy if the trend continues. The multidisciplinary team is tasked with the complex challenge of managing these interlinked complications, requiring ongoing reassessment and dynamic adaptation of the treatment plan. The emphasis remains on maintaining organ perfusion, managing the evolving respiratory and renal challenges, and vigilantly monitoring for signs of sepsis or multiorgan dysfunction syndrome (MODS), as the patient's critical journey continues.

Section 3

As the medical team continues to navigate the complex clinical picture, a new complication arises that demands immediate attention. The patient's respiratory status, though temporarily stabilized post-intubation, begins to show signs of further compromise. Serial chest x-rays reveal diffuse bilateral infiltrates, suggestive of acute respiratory distress syndrome (ARDS), likely secondary to the combined insult of inhalation injury and systemic inflammatory response. Ventilator settings are adjusted to a lung-protective strategy, with low tidal volumes and increased positive end-expiratory pressure (PEEP) to improve oxygenation and prevent further lung injury.

Concurrently, the patient's hemodynamic instability persists despite the initiation of vasopressor support. The mean arterial pressure struggles to stay above 60 mmHg, even with escalating doses of norepinephrine, signaling the possibility of refractory septic shock. Repeat lactate levels are elevated at 5.5 mmol/L, further indicating tissue hypoperfusion. The team decides to broaden antibiotic coverage and considers the addition of adjunctive therapies, such as corticosteroids, to modulate the inflammatory response.

Amidst these challenges, the declining renal function remains a critical concern. With creatinine levels climbing to 4.2 mg/dL and persistent oliguria, the nephrology team is consulted to discuss the initiation of continuous renal replacement therapy (CRRT), aiming to manage the severe electrolyte imbalances and fluid overload without compromising hemodynamic stability. The multidisciplinary team remains vigilant, ready to adapt the therapeutic approach as the patient teeters on the brink of multi-organ dysfunction syndrome, underscoring the necessity of precise clinical judgment and coordinated care in this precarious stage of recovery.

Section 4

The medical team faces a new development as the patient's neurological status begins to deteriorate. Initially responsive to painful stimuli, the patient now exhibits a Glasgow Coma Scale (GCS) score of 6, indicating a significant decline in consciousness. Pupillary assessment reveals anisocoria, with the left pupil larger and sluggishly reactive, raising concerns about potential increased intracranial pressure (ICP). In the context of the patient's critical illness, this neurological change prompts an urgent call to the neurology team for further evaluation and management.

Simultaneously, the latest lab results reveal a troubling metabolic acidosis with a pH of 7.22, bicarbonate level of 16 mmol/L, and an anion gap of 20, suggesting a mixed etiology. Given the patient's clinical picture, the team hypothesizes a combination of lactic acidosis from ongoing tissue hypoperfusion and renal failure, along with possible cerebral hypoxia contributing to the neurological decline. To address these multifaceted challenges, the intensivist suggests the insertion of an ICP monitor to guide the management of suspected cerebral edema, while the nephrology team accelerates plans for CRRT initiation to correct acid-base imbalances and support renal function.

In response to these developments, the care team emphasizes close monitoring of neurological signs, with frequent reassessment to detect any further changes. The patient's ventilator settings are carefully scrutinized to optimize cerebral perfusion, balancing oxygen delivery with the need to minimize further lung injury. As they navigate this critical juncture, the team remains acutely aware that every intervention must be delicately calibrated to stabilize the patient without tipping the balance toward further complications, underscoring the critical role of interdisciplinary collaboration and advanced clinical reasoning.

Section 5

As the critical care team continues to manage the patient's complex situation, a new set of diagnostic results arrives, providing further insight into the unfolding clinical picture. A repeat CT scan of the brain reveals evidence of diffuse cerebral edema, confirming the suspicion of increased intracranial pressure. This finding aligns with the earlier neurological assessment and further underscores the urgency of addressing potential cerebral hypoxia. Concurrently, an arterial blood gas analysis shows a pH of 7.18, PaCO2 of 56 mmHg, and PaO2 of 62 mmHg, indicating worsening respiratory acidosis alongside the metabolic derangements. These results suggest that despite adjustments to the ventilator settings, the patient's respiratory status is deteriorating, contributing to the overall acid-base imbalance.

In response to these findings, the multidisciplinary team ramps up efforts to stabilize the patient. The intensivist orders an immediate hypertonic saline infusion in an attempt to reduce cerebral edema and improve neurological status. Meanwhile, the nephrology team initiates continuous renal replacement therapy (CRRT) to address the worsening acidosis and support renal function. The patient's hemodynamic status is closely monitored, with norepinephrine titration to maintain adequate cerebral perfusion pressure. Despite these measures, the patient remains hemodynamically unstable, with a blood pressure of 88/54 mmHg and a heart rate of 124 beats per minute, indicating ongoing systemic challenges.

As the team navigates these critical interventions, they remain vigilant for new complications that may arise. The intensivist highlights the importance of maintaining delicate balance in fluid management to prevent exacerbating cerebral edema while ensuring adequate perfusion to vital organs. The nursing staff is tasked with frequent neurological assessments and continuous monitoring of vital signs, providing real-time data to guide clinical decisions. The integration of these complex interventions requires advanced clinical reasoning skills, as the team strives to stabilize the patient while anticipating potential setbacks in this high-stakes clinical scenario.