burns - Nursing Case Study

Pathophysiology

• Primary mechanism: Burn injury causes direct thermal damage to skin layers, leading to protein denaturation, cellular destruction, and disruption of skin's protective barrier, initiating an inflammatory response.

• Secondary mechanism: The inflammatory response triggers vasodilation and increased capillary permeability, resulting in fluid leakage into interstitial spaces, causing edema and potential hypovolemia.

• Key complication: Hypovolemic shock can occur due to significant fluid and electrolyte loss, reducing blood volume and impairing organ perfusion, necessitating prompt fluid resuscitation to prevent organ failure.

Patient Profile

Demographics:

34-year-old male, construction worker

History:

• Key past medical history: Hypertension, smoker for 10 years

• Current medications: Lisinopril 10 mg daily

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Severe burns on the left arm and hand

• Key symptoms: Intense pain, blistering, redness, swelling, limited mobility of the fingers, signs of infection (increased redness and warmth)

• Vital signs: Temperature 101.3°F, Heart rate 112 bpm, Blood pressure 145/92 mmHg, Respiratory rate 22 breaths per minute

Section 1

As the initial treatment began, the burn assessment revealed partial-thickness burns covering approximately 15% of the patient's total body surface area. The blistering and intense erythema over the left arm and hand were consistent with second-degree burns. The patient's vital signs indicated a systemic response to the injury, with elevated temperature and tachycardia pointing towards an infectious process or systemic inflammatory response. Blood cultures and wound swabs were obtained to identify potential pathogens, given the signs of infection around the burn area.

Laboratory results showed elevated white blood cell count (WBC 18,000/mm³) and C-reactive protein levels, suggesting an inflammatory or infectious process. Electrolyte analysis revealed hyponatremia (sodium level of 130 mmol/L) and hyperkalemia (potassium level of 5.5 mmol/L), likely resulting from tissue damage and fluid shifts. Renal function tests showed slightly elevated creatinine levels, hinting at early signs of acute kidney injury, possibly due to decreased renal perfusion and ongoing hypovolemia.

Despite initial fluid resuscitation efforts, the patient began showing signs of deteriorating status. His blood pressure dropped to 122/78 mmHg, and he exhibited increased confusion and restlessness. The decrease in blood pressure, coupled with altered mental status, raised concerns for progressing hypovolemic shock or sepsis. Given these changes, the clinical team intensified monitoring and adjusted the fluid management plan, while initiating broad-spectrum antibiotics to address potential infection while awaiting culture results. This strategic adjustment was crucial to stabilize the patient and prevent further complications, paving the way for the next phase of his recovery and treatment.

Section 2

As the clinical team continued to assess the patient's response to the interventions, new diagnostic results introduced additional concerns. The blood cultures returned positive for Staphylococcus aureus, confirming a bacterial infection that was likely contributing to the systemic inflammatory response. The presence of this pathogen, along with the patient's elevated temperature and tachycardia, indicated the progression to sepsis. In conjunction with the positive cultures, the wound swabs also showed heavy growth of the same bacteria, reinforcing the need for targeted antibiotic therapy. The antibiogram suggested sensitivity to vancomycin, prompting a change from broad-spectrum antibiotics to a more focused antimicrobial regimen to effectively combat the infection.

Further laboratory tests highlighted a worsening of the patient's electrolyte imbalances, with sodium levels dropping to 128 mmol/L and potassium increasing to 5.8 mmol/L. These changes, along with a creatinine level that had risen to 1.8 mg/dL, suggested a deterioration of renal function, likely exacerbated by the ongoing inflammatory process and inadequate renal perfusion. The patient's blood pressure continued to decline, now recorded at 115/75 mmHg, which, combined with his persistent confusion and restlessness, underscored the possibility of septic shock.

The clinical team recognized the need to escalate care to address these new complications, including the potential for acute kidney injury and worsening sepsis. They adjusted the fluid management strategy to include both crystalloids and colloids to enhance vascular volume, while also incorporating vasopressor support to maintain adequate blood pressure and organ perfusion. The initiation of renal protective strategies, alongside continuous monitoring of renal function and electrolytes, was deemed essential to mitigate further renal damage. These interventions were pivotal in stabilizing the patient, preparing him for potential transfer to a higher level of care should his condition not improve, and ensuring a comprehensive approach to his complex clinical needs.

Section 3

As the clinical team implemented the adjusted treatment plan, they closely monitored the patient for any changes in status. Over the next 12 hours, the patient's response to the targeted vancomycin regimen showed initial promise, with a slight reduction in fever and a stabilization of heart rate around 95 beats per minute. However, the patient's mental status remained a significant concern. Despite the stabilization of some vital signs, he continued to exhibit confusion and intermittent agitation, signaling that the underlying infectious process and inflammatory response were still exerting considerable strain on his system.

Subsequent laboratory tests revealed a mixed picture. While the white blood cell count began to decrease, indicating a potential response to the antibiotic therapy, new issues emerged. The patient's lactate level had risen to 4.0 mmol/L, a worrying sign that tissue hypoperfusion was persisting despite the vasopressor support and fluid resuscitation. The electrolyte imbalance remained problematic, with sodium levels falling further to 126 mmol/L and potassium creeping up to 6.0 mmol/L, heightening the risk of cardiac complications. Moreover, the creatinine level increased to 2.1 mg/dL, confirming the progression towards acute kidney injury.

Recognizing the need for a more aggressive approach to counteract these complications, the team explored additional interventions. They considered initiating continuous renal replacement therapy (CRRT) to address the electrolyte disturbances and support renal function. Moreover, they deliberated on the need for further imaging to rule out any underlying abscess formation or other complications that might be contributing to the persistent sepsis. The clinical team's decision-making process highlighted the importance of ongoing assessment and adaptation of the treatment plan to meet the evolving needs of the patient, underscoring the critical nature of timely and precise interventions in complex burn-related cases.

Section 4

As the clinical team proceeded with the decision to initiate continuous renal replacement therapy (CRRT), they aimed to address the patient's worsening electrolyte imbalances and support the failing renal function. Within the first few hours of CRRT initiation, the team observed a gradual improvement in the patient's electrolyte levels. Sodium levels began to correct, rising to 130 mmol/L, while potassium levels decreased to 5.4 mmol/L, reducing the immediate risk of cardiac complications. Despite these improvements, the patient's confusion remained unchanged, suggesting that factors beyond electrolyte imbalance were contributing to his altered mental status.

New diagnostic imaging was conducted to further investigate potential sources of persistent sepsis that might be complicating the recovery process. A CT scan of the abdomen and pelvis revealed a small intra-abdominal abscess, likely secondary to translocation of bacteria from the burn wounds. This finding necessitated a surgical consultation to evaluate the need for drainage or other interventions to control the infection. Concurrently, blood cultures were repeated to identify any resistant organisms or secondary infections that might not be covered by the current antibiotic regimen.

In response to these developments, the clinical team adjusted the treatment plan to incorporate targeted interventions aimed at resolving the abscess and fine-tuning antimicrobial therapy. The decision to broaden the spectrum of antibiotic coverage was based on the need to address potential polymicrobial infection until definitive culture results were available. This proactive approach, combined with ongoing CRRT, was critical to stabilizing the patient's condition and preventing further deterioration. As the patient continued to be closely monitored, the team remained vigilant for any signs of new complications, recognizing the delicate balance required to manage the multifaceted challenges of severe burn injuries and associated sepsis.

Section 5

Following the adjustments to the treatment plan, the clinical team observed a change in the patient's status within the next 24 hours. The patient's vital signs showed mixed changes: their heart rate decreased to 92 beats per minute from a previous tachycardic state, but the blood pressure remained borderline low at 90/58 mmHg. The respiratory rate was stable at 20 breaths per minute, and SpO2 levels were maintained at 95% on room air. Despite improved electrolyte levels, the patient's urine output remained minimal, indicating persistent renal challenges.

The surgical team evaluated the intra-abdominal abscess and decided that percutaneous drainage under ultrasound guidance was appropriate, given the patient's current hemodynamic stability and the size of the abscess. Post-procedure, the patient's white blood cell count decreased slightly from 15,000/mm³ to 13,500/mm³, suggesting a partial response to both the abscess drainage and the broadened antibiotic coverage. However, the patient's mental status remained an area of concern, with continued confusion and intermittent agitation. A further review of the patient's medication regimen revealed potential contributors to altered cognition, prompting the clinical team to reassess and adjust sedative dosages while ensuring adequate pain control.

Despite these interventions, new complications arose. Repeat blood cultures identified a multidrug-resistant organism, necessitating another shift in antibiotic therapy. The infectious disease specialist recommended the addition of a more targeted antimicrobial agent, pending sensitivity results. The patient's liver function tests began to show mild abnormalities, with an increase in bilirubin to 2.5 mg/dL and AST/ALT levels rising to 80/65 U/L, respectively, raising concerns about potential drug-induced liver injury or sepsis-related hepatopathy. These findings prompted discussions within the interdisciplinary team to carefully balance the benefits and risks of ongoing treatments, ensuring the comprehensive management of the patient's complex clinical picture. The team continued to monitor the patient's progress closely, ready to adapt the plan as new information emerged.