RSV - Nursing Case Study

Pathophysiology

• Primary mechanism: RSV attaches to epithelial cells in the respiratory tract, leading to cell fusion and formation of multinucleated giant cells (syncytia). This induces an inflammatory response, causing edema, increased mucus production, and reduced ciliary function, resulting in airway obstruction and impaired gas exchange.

• Secondary mechanism: The virus stimulates an immune response, leading to the release of cytokines and chemokines. This causes further inflammation, cell damage, and apoptosis, exacerbating respiratory symptoms.

• Key complication: Severe RSV infection can lead to bronchiolitis and pneumonia, which can cause hypoxemia and respiratory failure, particularly in infants and the elderly. Additionally, the exaggerated immune response can result in long-term airway hyperreactivity and recurrent wheezing.

Patient Profile

Demographics:

60-year-old male, retired coal miner

History:

• Key past medical history: Chronic obstructive pulmonary disease (COPD), type 2 diabetes, previous history of pneumonia

• Current medications: Metformin, Symbicort, Ventolin as needed

• Allergies: No known drug allergies

Current Presentation:

• Chief complaint: Severe shortness of breath, high fever

• Key symptoms: Productive cough with green sputum, fatigue, wheezing, chest tightness, loss of appetite

• Vital signs: Temperature - 103.5°F, Pulse - 115 beats per minute, Respiratory rate - 32 breaths per minute, Blood pressure - 160/90 mmHg, Oxygen Saturation - 88% on room air

Section 1

Change in Patient Status:

Overnight, the patient's condition worsens significantly. The night shift nurse reports that the patient is increasingly restless and agitated, with increased work of breathing. He remains febrile, with a temperature of 104°F. His respiratory rate has increased to 40 breaths per minute and pulse is now 130 beats per minute. Oxygen saturation levels have dropped to 82% on 5L of oxygen via nasal cannula. Blood pressure has increased to 170/95 mmHg. His cough has become more frequent and he reports increasing chest discomfort.

The patient is now demonstrating signs of severe respiratory distress. He is using accessory muscles to breathe and has developed bilateral wheezing and crackles. He appears cyanotic around his lips. The patient reports severe fatigue and is unable to complete full sentences due to his breathlessness. His blood glucose levels have also become unstable, with readings fluctuating between 180-250 mg/dL, likely due to the stress of his acute illness and corticosteroid use.

This deterioration in the patient's status indicates a progression of his RSV infection and possibly the development of complications such as pneumonia or acute respiratory distress syndrome (ARDS). This requires immediate intervention and reevaluation of his treatment plan. It also raises questions about his overall prognosis given his advanced age and comorbidities.

Section 2

New Diagnostic Results:

The patient’s blood culture results come back positive for Streptococcus pneumoniae, indicating a bacterial superinfection on top of his RSV infection. A chest X-ray further reveals diffuse infiltrates in both lungs consistent with ARDS. His arterial blood gas (ABG) results demonstrate a PaO2/FiO2 ratio of less than 200, confirming the presence of ARDS. His CO2 level is elevated at 55 mm Hg, indicating hypercapnia. The ABG also shows a decreased pH of 7.28, suggesting respiratory acidosis.

His complete blood count (CBC) shows a leukocytosis, with a white blood cell count of 18,000/uL, and the differential indicates a left shift with 85% neutrophils, suggesting an acute bacterial infection. The hemoglobin A1C is 8.5%, indicating poor glycemic control over the past three months. Elevated procalcitonin levels and C-reactive protein further corroborate the presence of a severe bacterial infection.

These new diagnostic results are alarming. They suggest that the patient’s RSV infection has escalated into a bacterial pneumonia, leading to ARDS. Given his advanced age, comorbidities, and now, ARDS, his prognosis becomes more uncertain. This calls for a rapid reassessment of the patient’s current treatment plan and consideration of more aggressive interventions, including possible intubation and mechanical ventilation.

Section 3

Change in Patient Status:

The patient's condition deteriorates rapidly over the next few hours. He develops a high fever of 103.2°F and his respiratory rate increases to 35 breaths per minute. His oxygen saturation dips to 88% on 6L nasal cannula. On physical examination, the patient appears lethargic and is noted to have increased work of breathing with use of accessory muscles and intercostal retractions. Crackles can be heard diffusely throughout both lungs, and his breath sounds are decreased in the lower lobes.

The patient’s mental status also begins to decline, as he becomes increasingly confused and disoriented. His Glasgow Coma Scale score falls to 11. His blood pressure is also noted to be on a downward trend, now measuring 90/60 mm Hg, and his heart rate has increased to 115 beats per minute. These signs collectively suggest that the patient is in septic shock, potentially due to the uncontrolled bacterial infection. His worsening hypoxia, coupled with his increased work of breathing, indicates that his respiratory status is also declining rapidly, suggesting that immediate intervention is necessary to prevent further deterioration.

Section 4

New Diagnostic Results:

The patient's laboratory results return, demonstrating elevated levels of C-reactive protein at 18mg/dL, and procalcitonin at 2.5 ng/mL, suggesting a severe systemic infection. His blood cultures from earlier are still pending. His arterial blood gas shows a pH of 7.30, PaCO2 of 50, PaO2 of 55, and bicarb of 24, indicating acute respiratory acidosis with hypoxemia. His complete blood count reveals a significantly elevated white blood cell count of 18,000 per microliter with a left shift, further supporting the suspicion of sepsis.

The chest x-ray reveals widespread bilateral infiltrates, suggesting the development of Acute Respiratory Distress Syndrome (ARDS), likely precipitated by the severe RSV infection and possible secondary bacterial infection. The echocardiogram shows a normal ejection fraction with no significant valvular abnormalities, indicating that his hypotension is likely due to sepsis-induced distributive shock, rather than cardiogenic shock.

These findings confirm the gravity of the patient's condition and necessitate aggressive critical care management. The patient's rapid clinical deterioration, coupled with his diagnostic results, indicates a transition into severe sepsis with ARDS. The team must act swiftly to stabilize the patient, while also considering the potential need for mechanical ventilation given his progressive respiratory failure. These results also suggest that broad-spectrum antibiotic coverage should be started immediately, pending the results of the blood cultures.

Section 5

New Complications:

In the early hours of the morning, the patient's condition worsens significantly. His respiratory rate escalates to 35 breaths per minute, and his SpO2 decreases to 88% on high-flow nasal cannula at 15 L/min and 60% FiO2. His blood pressure falls to 85/50 mmHg, and his heart rate increases to 125 beats per minute. He becomes increasingly lethargic and less responsive to verbal stimuli, raising concerns about potential hypoxic encephalopathy. A repeat arterial blood gas shows a worsening acidosis with a pH of 7.25, PaCO2 of 60, PaO2 of 50, and bicarb of 22.

The patient's worsening hypoxemia, despite escalating oxygen therapy, suggests refractory hypoxemia, a severe complication of ARDS. His decreasing blood pressure, despite fluid resuscitation, indicates that he may be progressing to septic shock. A bedside ultrasound reveals a dilated inferior vena cava with minimal variation during respiration, suggesting volume overload. This raises concerns about the potential onset of acute kidney injury due to septic shock, further complicating his medical management. The team decides to initiate vasopressor therapy and prepare for immediate intubation and mechanical ventilation. Concurrently, the nephrology team is consulted to consider the need for renal replacement therapy.