CLASBI - Nursing Case Study

Pathophysiology

• Primary mechanism: CLASBI, or Central Line-Associated Bloodstream Infection, primarily occurs when microorganisms, such as bacteria and fungi, gain direct access to the bloodstream via a central venous catheter. This breach in the sterile barrier can result from improper insertion techniques or inadequate maintenance of the catheter site.

• Secondary mechanism: Biofilm formation on the surface of the catheter is a critical factor. Microorganisms adhere to the catheter, creating a protective biofilm that shields them from both the host's immune defenses and antimicrobial agents, enabling persistent infection and complicating treatment.

• Key complication: Systemic infection can arise, leading to sepsis, which is characterized by a systemic inflammatory response that may progress to multi-organ dysfunction. Prompt recognition and management are essential to prevent severe outcomes.

Patient Profile

Demographics:

45-year-old female, school teacher

History:

• Key past medical history: Hypertension, Type 2 Diabetes, previous CLASBI episode 2 years ago

• Current medications: Lisinopril, Metformin, Aspirin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Fever and chills for the past 48 hours

• Key symptoms: Fatigue, redness and tenderness around catheter site, headache

• Vital signs: Temperature 101.3°F, Heart rate 110 bpm, Blood pressure 100/60 mmHg, Respiratory rate 22 breaths per minute

Section 1

New Diagnostic Results:

Following the initial assessment, additional diagnostic tests were performed to determine the extent of the infection and guide treatment. Blood cultures drawn from both the central line and a peripheral vein returned positive for Staphylococcus aureus, indicating a systemic infection. A complete blood count showed leukocytosis with a white blood cell count of 16,000/mm³, and the differential revealed a left shift, suggesting an acute bacterial infection. C-reactive protein and procalcitonin levels were elevated, further supporting an inflammatory response consistent with sepsis. An ultrasound of the catheter site was ordered to assess for any localized abscess formation, which showed increased echogenicity around the catheter, suggestive of early abscess development.

The patient's renal function tests revealed a mild increase in creatinine levels at 1.5 mg/dL, up from her baseline of 1.0 mg/dL, indicating potential renal involvement. Liver function tests remained within normal limits. Due to her history of diabetes, a glycated hemoglobin (HbA1c) test was conducted, revealing poor glycemic control with a value of 9.2%, which could impair her immune response and exacerbate infection risk. Given these results, the clinical team was concerned about the potential for rapid progression to more severe sepsis or septic shock, necessitating close monitoring and aggressive management.

The results of the diagnostics led to an immediate multidisciplinary team meeting to reassess the patient's treatment plan. The team decided to remove the infected central line and initiate broad-spectrum intravenous antibiotics, excluding penicillin due to her allergy, with plans to tailor the regimen based on culture sensitivities. The patient was also started on a fluid resuscitation protocol to address hypotension and was closely monitored for signs of organ dysfunction. With these interventions underway, the focus shifted to vigilant monitoring for any new complications or changes in the patient's status, as the potential for rapid clinical deterioration remained a significant concern.

Section 2

As the patient continued to receive treatment, her clinical status began to exhibit concerning changes. Despite the initiation of broad-spectrum antibiotics and fluid resuscitation, she developed new symptoms indicative of potential complications. The patient reported increased shortness of breath and displayed tachypnea, with a respiratory rate climbing to 28 breaths per minute. Her oxygen saturation dropped to 90% on room air, prompting the healthcare team to supplement her with oxygen via nasal cannula. Auscultation revealed diminished breath sounds and crackles at the bases of both lungs, raising suspicion for the development of pulmonary complications such as early acute respiratory distress syndrome (ARDS).

Concurrently, her hemodynamic status showed signs of worsening. Blood pressure readings, which had initially stabilized, began to trend downwards, with measurements around 88/54 mmHg despite ongoing fluid resuscitation efforts. Her heart rate increased to 118 beats per minute, indicating a compensatory response to hypotension. Repeat laboratory tests revealed a further increase in creatinine levels to 1.8 mg/dL, suggesting worsening renal impairment, while serum lactate levels rose to 3.5 mmol/L, confirming tissue hypoperfusion and indicating a progression towards septic shock.

These developments necessitated an urgent reassessment of the treatment strategy. The clinical team discussed escalating the level of care, considering the transfer to the intensive care unit for closer monitoring and potential initiation of vasopressors to maintain perfusion. Additional diagnostic imaging, such as a chest X-ray, was ordered to further evaluate the respiratory status and guide interventions. The multidisciplinary team emphasized the importance of ongoing re-evaluation of organ function and the need for dynamic adjustments to the patient's care plan to address the rapidly evolving clinical situation.

Section 3

Following the initial assessment and the concerning developments in the patient's condition, new diagnostic results provided further insights into her deteriorating status. The chest X-ray revealed bilateral infiltrates consistent with early acute respiratory distress syndrome (ARDS), confirming the team's suspicions based on the physical examination and respiratory symptoms. This finding underscored the significance of addressing her respiratory compromise promptly. Additionally, an echocardiogram was performed to assess cardiac function, which showed normal left ventricular ejection fraction but signs of mild right ventricular strain, possibly as a result of increased pulmonary pressures and hypoxia.

The laboratory workup was expanded to include a comprehensive metabolic panel and coagulation profile. Results indicated a worsening metabolic acidosis with a bicarbonate level of 18 mEq/L, an anion gap of 16, and an elevated prothrombin time of 18 seconds, suggesting the onset of coagulopathy, a common complication in severe sepsis and septic shock. These findings emphasized the potential need for blood product support and further hemodynamic stabilization.

Given these developments, the clinical team prioritized the escalation of care by transferring the patient to the intensive care unit (ICU). This move enabled continuous monitoring and the initiation of vasopressor therapy with norepinephrine to counteract persistent hypotension. The patient's care plan was adjusted to include low tidal volume mechanical ventilation to support her respiratory function while minimizing ventilator-induced lung injury. The multidisciplinary team, including critical care specialists, nephrologists, and infectious disease experts, convened to reassess antibiotic coverage, considering the possibility of multidrug-resistant organisms contributing to her condition. With these coordinated efforts, the focus remained on stabilizing the patient's condition, preventing further complications, and closely monitoring her response to the intensified treatment regimen.

Section 4

The patient's response to interventions over the following 24 hours was mixed, necessitating ongoing clinical vigilance and adaptive management. Despite the initiation of norepinephrine, her blood pressure remained labile, with readings fluctuating between 85/50 mmHg and 95/60 mmHg. This persistent hypotension highlighted the need for further evaluation of her fluid status. A point-of-care ultrasound was conducted, revealing a flat inferior vena cava suggestive of intravascular volume depletion, prompting the team to cautiously administer additional intravenous fluids while monitoring for signs of fluid overload.

Respiratory support with low tidal volume mechanical ventilation showed initial improvement in her oxygenation status, with arterial blood gases now demonstrating a PaO2 of 70 mmHg on 60% FiO2 and a PaCO2 of 45 mmHg, indicating adequate ventilation but ongoing hypoxemia. Despite this, the patient's oxygenation index remained borderline, warranting consideration of adjunctive therapies such as prone positioning or inhaled nitric oxide to enhance pulmonary function. Her metabolic acidosis persisted, though there was a slight improvement in bicarbonate levels to 20 mEq/L, suggesting a partial response to the interventions aimed at correcting her acid-base balance.

However, the emergence of a new complication became evident as the patient's urine output decreased significantly over the past few hours, with total output dropping to less than 200 mL in 24 hours despite adequate fluid resuscitation. This oliguria, coupled with rising serum creatinine levels now at 2.5 mg/dL from a baseline of 1.0 mg/dL, suggested the onset of acute kidney injury (AKI). The nephrology team was consulted to evaluate the need for renal replacement therapy, as the risk of fluid overload versus the necessity of maintaining adequate perfusion became a critical balancing act. The multidisciplinary team continued to prioritize a comprehensive approach, integrating these new developments into the ongoing assessment and adjustment of the patient's treatment plan.

Section 5

As the clinical team closely monitored the patient's condition, a critical change in her status emerged. Over the next 12 hours, the patient's respiratory function began to deteriorate despite ongoing mechanical ventilation and the consideration of adjunctive therapies. Her oxygen saturation dropped to 85% on an FiO2 of 70%, and her PaO2 decreased to 60 mmHg. This change prompted the team to implement prone positioning to improve alveolar recruitment and oxygenation. Despite these efforts, the patient continued to exhibit signs of respiratory distress, with an increased respiratory rate and use of accessory muscles. The potential for acute respiratory distress syndrome (ARDS) was considered, necessitating a reevaluation of her respiratory management strategy.

In parallel, the patient's renal function showed further decline, with serum creatinine rising to 3.2 mg/dL and continued oliguria. The nephrology team performed a thorough assessment, including a review of fluid balance and medication history, to determine contributing factors to the worsening AKI. The decision was made to initiate continuous renal replacement therapy (CRRT) to address the dual concerns of fluid overload and electrolyte imbalances, while also ensuring adequate removal of potential nephrotoxins. This intervention aimed to provide renal support while maintaining hemodynamic stability, a critical consideration given her ongoing hemodynamic lability.

The multidisciplinary team remained vigilant, integrating these new developments into the overall treatment plan. They continued to prioritize a balanced approach, carefully adjusting interventions to optimize organ function while avoiding complications. Regular team huddles were conducted to review the patient's progress, evaluate response to interventions, and explore additional therapeutic options. This dynamic and adaptive management approach underscored the complexity of the patient's condition, emphasizing the need for ongoing clinical reasoning and collaboration to navigate her challenging clinical course.