VAP - Nursing Case Study

Pathophysiology

• Primary mechanism: Ventilator-associated pneumonia (VAP) is mainly caused by bacterial colonization in the trachea. Prolonged mechanical ventilation disrupts the normal defense mechanisms of the respiratory tract, facilitating the entry and multiplication of pathogenic bacteria.

• Secondary mechanism: Micro-aspiration of contaminated secretions into the lower respiratory tract is another crucial mechanism. Despite preventative measures, micro-aspiration often occurs due to the presence of an endotracheal or tracheostomy tube.

• Key complication: VAP may lead to severe complications like sepsis and acute respiratory distress syndrome. These complications are associated with significant mortality, prolonged ICU stay, and increased healthcare costs.

Patient Profile

Demographics:

67-year-old male, retired coal miner

History:

• Key past medical history: Chronic Obstructive Pulmonary Disease (COPD), hypertension, type 2 diabetes mellitus, and a history of smoking.

• Current medications: Metformin, Lisinopril, Salmeterol, and Tiotropium.

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Difficulty in breathing, persistent cough with greenish sputum.

• Key symptoms: Fever, chills, purulent sputum, increasing shortness of breath, fatigue, and confusion.

• Vital signs: Temperature 39.2°C (102.5°F), heart rate 125 bpm, blood pressure 90/60 mmHg, respiratory rate 30 breaths per minute, oxygen saturation 88% on room air.

Section 1

Change in Patient Status:

Over the next 24 hours, the patient's condition worsens significantly. His oxygen saturation drops to 84% on room air, and he becomes increasingly tachypneic with a respiratory rate of 35 breaths per minute. His heart rate continues to increase to 135 bpm, and blood pressure falls further to 85/50 mmHg. He develops a new onset of severe agitation and restlessness. Auscultation of the chest reveals decreased breath sounds and coarse crackles bilaterally, suggesting a deteriorating respiratory status. Additionally, his consciousness level decreases, as evidenced by a Glasgow Coma Scale score of 9 (E2V3M4), indicating a significant cognitive decline from his baseline.

New Diagnostic Results:

Given the patient's deteriorating condition, additional diagnostic tests are ordered. His arterial blood gas (ABG) shows a pH of 7.28, PaCO2 of 55 mmHg, PaO2 of 62 mmHg, and HCO3 of 24 mmol/L, indicative of acute respiratory acidosis. His white blood cell count has increased to 18,000 cells/µL, with a significant left shift. Blood cultures are drawn, which later confirm the presence of methicillin-resistant Staphylococcus aureus (MRSA). A chest X-ray reveals new bilateral infiltrates, further supporting the diagnosis of VAP. His worsening hypoxemia, agitation, and confusion may suggest the development of hypoxic encephalopathy, a serious complication of severe respiratory failure.

Section 2

New Complications:

As the patient's condition continues to deteriorate, new complications emerge. He becomes febrile with a temperature of 38.9°C, suggesting a systemic inflammatory response. Furthermore, he begins to exhibit signs of renal dysfunction, with a sharp increase in his serum creatinine to 2.5 mg/dL from a baseline of 0.9 mg/dL and a decrease in urine output to less than 0.5 mL/kg/hr despite adequate fluid resuscitation. His BUN also rises to 32 mg/dL, and labs reveal a decreased eGFR. These findings raise concern for acute kidney injury (AKI), possibly secondary to sepsis from the MRSA bacteremia.

Response to Interventions:

Despite the administration of broad-spectrum antibiotics, the patient's clinical status does not improve as expected. His tachypnea and hypoxemia persist, suggesting refractory respiratory failure. Given his worsening mental status and inability to protect his airway, the decision is made to proceed with endotracheal intubation and mechanical ventilation. However, the patient's hemodynamics continue to be unstable, requiring initiation of vasopressor support with norepinephrine. The nephrology team is consulted for the AKI, and renal replacement therapy is considered due to the lack of response to initial resuscitative measures and the progressive nature of his renal dysfunction. This case, thus, requires advanced clinical reasoning, as the complexity of the patient's condition necessitates critical decision-making and inter-professional collaboration.

Section 3

Change in Patient Status:

In the following days, the patient's already deteriorating condition takes a turn for the worse. His oxygen saturation levels continue to drop, dipping below 90% on 100% FiO2, and his PaO2/FiO2 ratio falls to 120, suggesting the development of acute respiratory distress syndrome (ARDS). Moreover, his respiratory acidosis worsens, with arterial blood gases showing a pH of 7.28 and a PaCO2 of 58 mm Hg. His GCS score also continues to decline, reaching a critical low of 6 - indicative of a significant reduction in his level of consciousness.

New Complications:

As the patient's respiratory status worsens, so too does his renal function. His serum creatinine further increases to 3.5 mg/dL and his urine output remains consistently below 0.5 mL/kg/hr. Additionally, his potassium levels surge to 5.8 mEq/L, and his serum bicarbonate drops to 18 mEq/L, suggesting metabolic acidosis likely secondary to his worsening renal function. Furthermore, despite vasopressor support, the patient's blood pressure remains stubbornly low with systolic pressure hovering around 90 mm Hg and diastolic pressure around 60 mm Hg. These new developments not only underscore the severity of the patient's condition but also necessitate the need for urgent, critical decision-making and a multidisciplinary approach to his care.

Section 4

Change in Patient Status:

Over the next 48 hours, the patient's condition further deteriorates. His oxygen saturation levels continue to drop alarmingly, falling below 90% even with 100% FiO2 and necessitating the need for mechanical ventilation. His Glasgow Coma Scale score further declines to 5, indicative of a severe decrease in his level of consciousness. The patient's blood pressure remains critically low, with systolic pressure consistently under 90 mm Hg and diastolic pressure around 55 mm Hg. His heart rate also increases to 120 beats per minute, suggestive of compensatory tachycardia.

New Complications:

The patient's worsening condition is further complicated by the development of severe sepsis with multiple organ dysfunction syndrome (MODS). His serum lactate levels rise to 4.5 mmol/L, indicative of tissue hypoperfusion. Additionally, his platelet count decreases to 50,000 per microliter, suggestive of disseminated intravascular coagulation (DIC). The patient's renal function continues to decline, with his serum creatinine rising to 4.2 mg/dL and urine output decreasing to less than 0.3 mL/kg/hr. His potassium levels continue to surge, reaching a critical level of 6.0 mEq/L. The patient's worsening condition necessitates a more aggressive and multidisciplinary approach to his care, with a focus on hemodynamic stabilization, organ support, and targeted antimicrobial therapy.

Section 5

Change in Patient Status:

Despite aggressive management, the patient's condition further declines in the ensuing 24 hours. His oxygenation remains critically low, with an oxygen saturation level of 88% on 100% FiO2 and mechanical ventilation. His Glasgow Coma Scale score reduces to 3, indicating a profound decrease in his consciousness level. His blood pressure continues to plummet, with systolic readings dropping to 85 mm Hg and diastolic readings hovering around 50 mm Hg. His heart rate escalates to 130 beats per minute, indicative of worsening compensatory tachycardia. The patient also begins to exhibit signs of respiratory distress, with an increased respiratory rate of 30 breaths per minute and the use of accessory muscles.

New Diagnostic Results:

The patient's deteriorating condition is supported by alarming laboratory results. His serum lactate levels spike to 6.0 mmol/L, suggesting worsening tissue hypoperfusion. His platelet count further drops to 30,000 per microliter, indicative of progressive DIC. His renal function further declines, with a serum creatinine level of 5.0 mg/dL and a urine output of less than 0.2 mL/kg/hr. His potassium levels further rise, reaching a dangerous level of 6.5 mEq/L. Additionally, his liver function tests show a marked increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, suggestive of liver involvement. The patient's worsening clinical and laboratory parameters demand immediate critical care interventions and a thorough reevaluation of his therapeutic strategy.