Burns - Nursing Case Study

Pathophysiology

• Primary mechanism: Thermal injury leads to protein denaturation and cell membrane disruption, causing immediate coagulative necrosis and initiating an inflammatory response that increases vascular permeability and fluid loss.

• Secondary mechanism: Systemic inflammatory response syndrome (SIRS) can develop from the release of cytokines and inflammatory mediators, leading to widespread endothelial injury, capillary leak syndrome, and subsequent hypovolemic shock.

• Key complication: Burn wound sepsis is a critical risk due to compromised skin barrier and immune dysregulation, potentially resulting in multi-organ dysfunction syndrome (MODS) if systemic infection ensues.

Patient Profile

Demographics:

45-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Lisinopril, Metformin, Insulin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe burns sustained in a workplace accident

• Key symptoms: Extensive burns covering 50% of body surface area, severe pain, difficulty breathing, decreased urine output

• Vital signs: Temperature 101.3°F, Heart rate 130 bpm, Respiratory rate 28 breaths/min, Blood pressure 88/54 mmHg, Oxygen saturation 85% on room air

Section 1

New Diagnostic Results:

Following the initial assessment, the patient underwent a series of diagnostic tests to further evaluate the extent of his injuries and the emerging complications. Laboratory results revealed significant abnormalities: a complete blood count showed leukocytosis with a white blood cell count of 18,000/mm³, suggesting an active inflammatory or infectious process. Serum lactate levels were elevated at 4.8 mmol/L, indicative of tissue hypoperfusion and possible sepsis. Blood cultures were obtained and revealed growth of Staphylococcus aureus, confirming the onset of burn wound sepsis. Kidney function tests showed elevated creatinine at 2.1 mg/dL and blood urea nitrogen (BUN) at 45 mg/dL, reflecting acute kidney injury likely secondary to hypovolemia and systemic inflammatory response.

The patient's chest X-ray highlighted bilateral pulmonary infiltrates, raising concerns for acute respiratory distress syndrome (ARDS) as a complication of the systemic inflammatory response syndrome (SIRS). Arterial blood gases showed a pH of 7.29, PaCO2 of 58 mmHg, and PaO2 of 60 mmHg, consistent with respiratory acidosis and hypoxemia. This combination of diagnostic findings suggests a progression to multi-organ dysfunction syndrome (MODS), necessitating immediate and aggressive intervention to stabilize the patient.

These diagnostic results prompt a critical reassessment of the treatment plan. The healthcare team must prioritize aggressive fluid resuscitation to combat hypovolemic shock, initiate broad-spectrum antibiotics tailored to the culture results to address the infection, and consider ventilatory support to manage respiratory failure. The emerging complications underscore the need for continuous monitoring and a multidisciplinary approach to care, emphasizing the importance of timely interventions and the potential need for renal replacement therapy if kidney function continues to decline. As the patient's condition evolves, ongoing evaluation and adaptation of the therapeutic strategy will be crucial in mitigating further deterioration and optimizing outcomes.

Section 2

Change in Patient Status:

Despite the aggressive fluid resuscitation initiated to address hypovolemic shock, the patient's condition has further deteriorated over the past 24 hours. Vital signs reveal a persistent tachycardia with a heart rate of 130 beats per minute, hypotension with a blood pressure of 86/54 mmHg, and a febrile state with a temperature of 39.2°C (102.6°F). The patient's urine output has dramatically decreased to less than 0.3 mL/kg/hour, signaling worsening renal function and potential progression to acute renal failure. Neurologically, the patient displays signs of altered mental status, with increased confusion and lethargy, likely due to cerebral hypoperfusion and systemic toxicity.

In response to the continued decline, the healthcare team has escalated care by initiating continuous renal replacement therapy (CRRT) to address the acute kidney injury and manage the fluid overload. Concurrently, the patient has been intubated and placed on mechanical ventilation due to the worsening respiratory status and to correct the severe respiratory acidosis. Ventilator settings have been adjusted to optimize oxygenation and reduce the risk of ventilator-associated lung injury. Despite these interventions, arterial blood gases reveal persistent metabolic acidosis with a pH of 7.25, HCO3- of 15 mEq/L, and a base excess of -10 mmol/L, indicating the need for further metabolic support.

The multidisciplinary team, including intensivists, nephrologists, and infectious disease specialists, convenes to reassess the treatment plan and explore additional therapeutic options, such as the potential use of vasopressors to support hemodynamics and the reconsideration of the antibiotic regimen to ensure optimal coverage against multi-drug resistant organisms. The patient's rapidly evolving clinical picture highlights the precarious balance of managing complex, interrelated systems, emphasizing the necessity for vigilant monitoring, timely interventions, and adaptive strategies to navigate the challenges of multi-organ dysfunction syndrome.

Section 3

New Diagnostic Results:

In the wake of the patient's deteriorating condition, additional diagnostic tests were conducted to elucidate the underlying issues contributing to the multi-organ dysfunction. The latest laboratory results reveal a marked leukocytosis, with a white blood cell count of 24,000/mm³, suggestive of an ongoing infectious process. Blood cultures have returned positive for Pseudomonas aeruginosa, a notoriously difficult organism to treat due to its propensity for multi-drug resistance. Sensitivity testing indicates resistance to several commonly used antibiotics, prompting the infectious disease team to recommend a shift to a more targeted antibiotic regimen, including the use of ceftolozane-tazobactam in combination with amikacin for enhanced coverage.

Further complicating the clinical picture, a chest X-ray and subsequent CT scan of the thorax reveal progressive bilateral infiltrates consistent with acute respiratory distress syndrome (ARDS), necessitating further adjustments to the mechanical ventilation strategy to improve oxygenation while minimizing barotrauma. The patient's central venous pressure (CVP) measurements remain elevated at 14 mmHg, indicating a state of fluid overload despite controlled fluid administration, likely exacerbated by capillary leak syndrome secondary to systemic inflammation.

The interdisciplinary team must now integrate these new findings into the existing treatment plan, balancing the need for aggressive infection control with the management of ARDS and fluid status to prevent further decompensation. This complex scenario demands constant reassessment of therapeutic efficacy and side effects, with an emphasis on early recognition of any new complications, such as septic shock or worsening organ dysfunction, to tailor interventions promptly and effectively.

Section 4

Change in Patient Status:

In the hours following the initiation of the new antibiotic regimen, the patient exhibits subtle yet concerning changes in clinical status that warrant immediate attention. Although the targeted therapy against Pseudomonas aeruginosa was anticipated to stabilize the infectious process, the patient's vital signs reveal a spike in heart rate to 130 beats per minute and a drop in mean arterial pressure to 60 mmHg, suggesting the early onset of septic shock. The patient's skin is noted to be cool and mottled, and capillary refill time has increased to over four seconds, indicating compromised peripheral perfusion.

Concurrently, the patient's respiratory status continues to decline despite adjustments in ventilatory support. Arterial blood gas analysis shows a worsening of hypoxemia, with a PaO2 of 55 mmHg and an increased PaCO2 of 60 mmHg, reflecting significant ventilation-perfusion mismatch and respiratory acidosis. The decision is made to escalate mechanical ventilation settings, incorporating a higher positive end-expiratory pressure (PEEP) to recruit collapsed alveoli, while cautiously monitoring hemodynamic status to prevent further cardiovascular instability.

Given these developments, the interdisciplinary team must swiftly reassess the current treatment strategy. The critical balance between managing infection, optimizing oxygenation, and supporting hemodynamics is paramount. Additional interventions such as the initiation of vasopressors may be necessary to maintain adequate blood pressure and organ perfusion. Furthermore, the team must anticipate potential complications from increased ventilatory pressures, including barotrauma and volutrauma, necessitating vigilant monitoring and frequent reassessment of the patient's evolving status. This escalation sets the stage for further diagnostic evaluations to determine the next steps in managing this complex, evolving clinical picture.

Section 5

With the patient's condition deteriorating, the interdisciplinary team decides to perform a bedside echocardiogram and repeat laboratory evaluations to gain further insights into the underlying complications. The echocardiogram reveals decreased left ventricular function, with an ejection fraction of 35%, suggesting cardiogenic involvement in the patient's hemodynamic instability. This finding, coupled with the hypotension and tachycardia, indicates a possible overlap of septic and cardiogenic shock, complicating the clinical management.

Laboratory tests reveal a significant elevation in lactate levels to 5 mmol/L, reinforcing concerns about tissue hypoperfusion and the likelihood of multi-organ dysfunction. Additionally, complete blood count results show a marked leukocytosis with a left shift, consistent with ongoing systemic infection and inflammatory response. Blood cultures are pending, but the team is highly suspicious of antibiotic resistance or a secondary infection complicating the primary Pseudomonas aeruginosa sepsis.

In response to these findings, the decision is made to initiate a low-dose inotropic agent to support cardiac output while continuing fluid resuscitation cautiously, given the risk of fluid overload in the context of reduced cardiac function. The team also considers the potential need for renal replacement therapy, as urine output has decreased to less than 0.5 mL/kg/hr, indicative of acute kidney injury. The complexity of the case now requires meticulous coordination among intensivists, cardiologists, nephrologists, and infectious disease specialists to tailor a comprehensive, dynamic treatment plan that addresses the multifaceted challenges presented by this rapidly evolving clinical scenario.