burns - Nursing Case Study

Pathophysiology

• Primary mechanism: Thermal injury causes direct damage to skin and underlying tissues, leading to protein denaturation and cell death. This disrupts the skin's barrier function, resulting in fluid loss and increased risk of infection.

• Secondary mechanism: Inflammatory response triggers the release of cytokines and vasoactive mediators, causing systemic capillary leak syndrome. This leads to hypovolemia, edema, and possible multi-organ dysfunction due to inadequate perfusion and oxygenation.

• Key complication: Severe burns can result in burn shock, characterized by a combination of hypovolemic and distributive shock, necessitating aggressive fluid resuscitation to prevent organ failure and promote tissue recovery.

Patient Profile

Demographics:

34-year-old male, firefighter

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Lisinopril, Metformin, Insulin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe burns sustained during a rescue operation

• Key symptoms: Extensive third-degree burns over 50% of body surface area, severe pain, difficulty breathing, altered mental status

• Vital signs: Temperature 102°F, Heart Rate 140 bpm, Respiratory Rate 32 breaths/min, Blood Pressure 85/50 mmHg, SpO2 88% on room air

Section 1

Change in Patient Status:

Shortly after arrival to the burn unit, the patient demonstrated a significant change in status. Despite aggressive fluid resuscitation following the Parkland formula, his blood pressure remained critically low at 80/45 mmHg, prompting concerns about refractory burn shock. His heart rate increased to 150 bpm, and his respiratory rate rose to 36 breaths per minute, with increasing accessory muscle use suggesting respiratory distress. Arterial blood gas analysis revealed a pH of 7.28, PaCO2 of 58 mmHg, and PaO2 of 60 mmHg, indicating a combined metabolic and respiratory acidosis. These findings were consistent with deteriorating respiratory function and inadequate tissue perfusion, necessitating immediate intervention to address both oxygenation and perfusion deficits.

The patient's altered mental status progressed to a semi-comatose state, with a Glasgow Coma Scale score dropping to 8, further complicating the clinical picture. Given the extensive facial burns and evidence of inhalation injury, there was a high suspicion of airway compromise. Fiberoptic bronchoscopy was performed, revealing significant airway edema and soot deposition, confirming inhalation injury. This discovery necessitated urgent endotracheal intubation to secure the airway and facilitate mechanical ventilation. The critical care team initiated protective lung ventilation strategies to address the acute respiratory failure and prevent further lung injury.

The patient's evolving hemodynamic instability and deteriorating respiratory status raised the possibility of developing Acute Respiratory Distress Syndrome (ARDS) and multi-organ dysfunction syndrome (MODS). These complications underscored the need for continuous monitoring and advanced critical care interventions, including vasopressor support and potential renal replacement therapy, to support organ function and optimize recovery. This change in status challenged the clinical team to reassess their approach and adapt the treatment plan to address the complex interplay of respiratory compromise, shock, and systemic inflammation.

Section 2

Response to Interventions:

Despite the initiation of mechanical ventilation and vasopressor support, the patient's condition continued to deteriorate. The critical care team implemented a norepinephrine infusion, titrated to maintain a mean arterial pressure above 65 mmHg. However, the patient's hemodynamic status remained unstable, with fluctuating blood pressures and persistent tachycardia at 145 bpm. Repeat arterial blood gas analysis showed minimal improvement with a pH of 7.30, PaCO2 of 55 mmHg, and PaO2 of 65 mmHg, indicating ongoing respiratory compromise despite ventilatory support. The lactate level was elevated at 5.5 mmol/L, suggesting inadequate perfusion and tissue hypoxia.

In response to the patient's deteriorating renal function, evidenced by rising creatinine levels at 2.1 mg/dL and decreasing urine output to less than 0.3 mL/kg/hr, the team initiated continuous renal replacement therapy (CRRT). This decision was made to manage fluid overload and support renal function, given the patient's oliguric state and fluid resuscitation needs. Despite these interventions, the patient developed new-onset atrial fibrillation, further complicating the clinical picture. This arrhythmia required the addition of amiodarone infusion to the treatment regimen to control the heart rate and prevent hemodynamic compromise.

As the patient's condition progressed, the clinical team remained vigilant for signs of multi-organ dysfunction syndrome (MODS), characterized by worsening liver function tests with elevated AST and ALT levels, as well as coagulopathy with an INR of 2.0. The possibility of disseminated intravascular coagulation (DIC) emerged, prompting the initiation of fresh frozen plasma and platelet transfusions to address the coagulation abnormalities. The complexity of the patient's condition necessitated frequent reassessment and adjustments to the therapeutic approach, highlighting the challenges of managing severe burn injuries complicated by systemic inflammatory response and organ dysfunction. The team's focus remained on stabilizing the patient while preventing further complications, emphasizing the critical need for continuous monitoring and advanced support measures.

Section 3

As the clinical team continued to manage the complex condition of the patient, new diagnostic results revealed further deterioration in the patient's status. A follow-up chest X-ray showed progressive bilateral infiltrates, consistent with acute respiratory distress syndrome (ARDS), adding another layer of complexity to the respiratory challenges already faced. The CT scan of the abdomen, performed due to increasing abdominal distension and tenderness, identified significant bowel edema and early signs of ischemia, raising the concern for impending abdominal compartment syndrome. This finding necessitated a multidisciplinary discussion about the potential need for surgical intervention to relieve intra-abdominal pressure and prevent further organ compromise.

Laboratory tests indicated worsening metabolic acidosis with a pH dropping to 7.25, despite maximal ventilatory support and bicarbonate administration. The patient's lactate level continued to climb, now at 7.2 mmol/L, underscoring the severity of systemic hypoperfusion. Liver function tests showed a marked increase, with AST and ALT levels tripling from previous values, suggesting acute hepatic injury likely secondary to hypoperfusion and systemic inflammatory response. The patient's renal function showed no improvement despite CRRT, with creatinine levels escalating to 3.5 mg/dL and urine output remaining critically low. These findings prompted the team to prioritize optimizing hemodynamic support and reassess the current fluid management strategy, considering the delicate balance needed to avoid exacerbating fluid overload while ensuring adequate perfusion.

The new onset of neurological changes, evidenced by decreased responsiveness and a Glasgow Coma Scale (GCS) score of 8, raised alarms for potential central nervous system involvement, possibly due to hypoxic brain injury or metabolic encephalopathy. The team initiated further neurological assessments, including an urgent CT scan of the head, to rule out intracranial pathology. These developments highlighted the need for reevaluation of treatment priorities, focusing on aggressive management of MODS and intensive monitoring to guide ongoing therapeutic decisions. The complexity of this patient's condition required an integrated, dynamic approach to care, with the recognition that each intervention could have far-reaching implications on the delicate balance of the patient's overall health status.

Section 4

As the medical team continued to address the patient's complex condition, a new complication emerged, further challenging the clinical management strategy. The patient's neurological status deteriorated rapidly, with a Glasgow Coma Scale (GCS) score now slipping to 6, indicating a severe level of impairment. The urgent CT scan of the head revealed diffuse cerebral edema, without any evident mass effect or hemorrhage, suggesting a possible hypoxic-ischemic injury compounded by metabolic encephalopathy. This finding necessitated immediate intervention to mitigate intracranial pressure and prevent further neurological compromise. Mannitol and hypertonic saline were administered as part of a targeted strategy to reduce cerebral edema, while the intensivist team closely monitored for any signs of improvement or further decline.

In parallel, the patient's hemodynamic stability remained precarious. Despite aggressive fluid resuscitation and vasopressor support, the mean arterial pressure hovered around 55 mmHg, indicating persistent shock. A repeat echocardiogram showed a decreased ejection fraction of 35%, suggesting a component of cardiogenic shock contributing to the systemic hypoperfusion. The decision was made to introduce an inotropic agent, dobutamine, to improve cardiac output and support systemic circulation. This intervention required careful titration and continuous hemodynamic monitoring to evaluate its efficacy and avoid exacerbating the patient's fluid overload and pulmonary status.

As these interventions unfolded, the patient's metabolic acidosis showed slight improvement, with the pH rising to 7.30. However, lactate levels remained elevated at 6.8 mmol/L, reflecting ongoing tissue hypoxia. The critical care team recognized the need for ongoing reassessment of the patient's comprehensive management plan, balancing the demands of treating multisystem organ dysfunction syndrome (MODS) against the risks of potential side effects from the aggressive interventions being employed. Multidisciplinary team discussions focused on dynamic treatment strategies, prioritizing interventions that could offer the greatest potential for stabilizing the patient's precarious condition, while remaining vigilant for any new complications that might arise.

Section 5

As the critical care team continued to monitor the patient, new diagnostic results brought additional challenges to the forefront. Blood cultures drawn earlier confirmed the presence of a multidrug-resistant Pseudomonas aeruginosa infection. The infectious disease specialists recommended initiating a combination antibiotic therapy tailored to the sensitivities of the identified strain. However, the team faced a dilemma: the nephrotoxic potential of the chosen antibiotics could exacerbate the patient’s already compromised renal function, evidenced by rising creatinine levels, now at 2.5 mg/dL, and a decreased urine output of less than 0.3 mL/kg/hr. These findings suggested an acute kidney injury (AKI) superimposed on the patient’s existing condition, complicating the balance between effective infection control and renal preservation.

Concurrently, the patient's respiratory status began to deteriorate, with increasing oxygen requirements and development of bilateral infiltrates on a follow-up chest X-ray, raising concerns for acute respiratory distress syndrome (ARDS). The ventilator settings were adjusted to a lung-protective strategy, emphasizing low tidal volumes and adequate positive end-expiratory pressure (PEEP) to prevent barotrauma while maintaining adequate oxygenation. Despite these adjustments, the patient's arterial blood gas showed a PaO2/FiO2 ratio of 150, indicative of moderate ARDS, necessitating consideration of adjunctive treatments such as prone positioning or extracorporeal membrane oxygenation (ECMO) if conventional strategies failed.

Amidst these developments, the multidisciplinary team reevaluated the overall management plan. The focus shifted to optimizing organ support while considering the risk-to-benefit ratio of each intervention. Emphasis was placed on dynamic assessment and early identification of any new complications, ensuring prompt, evidence-based adjustments to the therapeutic approach. This comprehensive and adaptive strategy aimed to navigate the complexities of the patient's critical condition, striving for stabilization and gradual recovery.