pneumonia - Nursing Case Study

Pathophysiology

• Primary mechanism: Pneumonia begins with the invasion of the lower respiratory tract by pathogens such as bacteria, viruses, or fungi, leading to an infection. This triggers an inflammatory response in the alveoli, causing them to fill with fluid and pus, which impairs gas exchange and results in symptoms like cough, fever, and difficulty breathing.

• Secondary mechanism: The inflammatory response also recruits immune cells, including neutrophils, to the site of infection. This can exacerbate tissue damage and edema, further hindering lung function and potentially leading to respiratory distress.

• Key complication: If untreated or severe, pneumonia can lead to acute respiratory failure, where the lungs cannot provide sufficient oxygen to the blood, or sepsis, a systemic inflammatory response to infection that can cause multi-organ failure.

Patient Profile

Demographics:

52-year-old male, construction worker

History:

• Key past medical history: Hypertension, Type 2 Diabetes

• Current medications: Lisinopril, Metformin

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Persistent cough and shortness of breath

• Key symptoms: Fever, productive cough with green sputum, chest pain, fatigue

• Vital signs: Temperature 101.8°F, Heart rate 112 bpm, Blood pressure 138/85 mmHg, Respiratory rate 26 breaths per minute, Oxygen saturation 88% on room air

Section 1

Change in Patient Status:

During the initial 24 hours of hospitalization, the patient, Mr. Thompson, exhibits signs of clinical deterioration. Overnight, his respiratory distress worsens, with an increased respiratory rate of 32 breaths per minute and a further drop in oxygen saturation to 84% despite supplemental oxygen via nasal cannula at 3 liters per minute. The patient's mental status also changes, becoming lethargic and less responsive to verbal stimuli, suggesting potential hypoxemia or the onset of sepsis-related encephalopathy. His heart rate remains elevated at 118 bpm, and he becomes hypotensive, with blood pressure readings dropping to 105/68 mmHg. These changes indicate a progression from localized pneumonia to potential systemic involvement, raising concerns about the development of sepsis or acute respiratory failure.

In response to these alarming changes, the healthcare team initiates a more aggressive management plan. The patient is transferred to the intensive care unit for closer monitoring and possible escalation of respiratory support. Arterial blood gas analysis reveals a PaO2 of 58 mmHg and an elevated PaCO2 of 52 mmHg, confirming acute respiratory failure. Blood cultures and a comprehensive metabolic panel are ordered to identify any infectious agents and assess organ function. Immediate interventions include initiating broad-spectrum intravenous antibiotics that are non-penicillin-based due to his allergy, increasing the oxygen supply, and considering non-invasive ventilation options. The team also begins fluid resuscitation to address the hypotension and performs a sepsis workup to guide further management. These measures aim to stabilize the patient and prevent further complications, such as multi-organ failure, while the clinical team awaits additional diagnostic results.

Section 2

New Diagnostic Results:

Following the initiation of the aggressive management plan, the laboratory results begin to trickle in, providing critical insights into Mr. Thompson's current condition. The blood cultures reveal the presence of Streptococcus pneumoniae, confirming the bacterial etiology of his pneumonia and guiding the choice of targeted antibiotic therapy. The comprehensive metabolic panel indicates a serum lactate level of 3.5 mmol/L, suggesting tissue hypoperfusion and supporting the suspicion of sepsis. Meanwhile, the liver function tests show mild elevations in AST and ALT, hinting at possible hepatic involvement, either from hypoperfusion or a developing systemic inflammatory response.

The arterial blood gas analysis, repeated after the initiation of non-invasive ventilation, shows a slight improvement in oxygenation with a PaO2 of 65 mmHg. However, the PaCO2 remains elevated at 50 mmHg, indicating ongoing respiratory compromise. The full blood count reveals leukocytosis with a left shift, consistent with an acute infectious process, while the procalcitonin level is elevated, further corroborating the diagnosis of sepsis.

With these results, the healthcare team decides to adjust the antibiotic regimen to include ceftriaxone and azithromycin, given the pneumococcal infection and the patient's penicillin allergy. The decision to continue non-invasive ventilation is reassessed, with a plan to intubate if the patient's respiratory status does not improve. Fluid resuscitation is titrated carefully, balancing the need to improve perfusion with the risk of fluid overload. These diagnostic findings and subsequent management adjustments are crucial in steering Mr. Thompson's treatment plan, aiming to stabilize his condition and prevent further complications, such as acute kidney injury or worsening respiratory failure. The team remains vigilant, monitoring for any additional symptoms that might indicate the need for further intervention.

Section 3

Change in Patient Status:

Despite the implementation of the adjusted management plan, Mr. Thompson's condition takes a concerning turn. Over the next 12 hours, his respiratory status deteriorates further. His vital signs reveal a persistent fever of 39.2°C (102.6°F), heart rate climbing to 120 bpm, and blood pressure dropping to 88/56 mmHg, indicating a hemodynamic instability consistent with septic shock. His respiratory rate increases to 32 breaths per minute, and he begins to exhibit increased work of breathing with pronounced use of accessory muscles and intercostal retractions, signaling impending respiratory failure. Although non-invasive ventilation initially provided some relief, it is now insufficient to meet his respiratory demands.

The medical team conducts a thorough reassessment and, given the escalation of his condition, decides to proceed with intubation and mechanical ventilation to secure his airway and ensure adequate gas exchange. Concurrently, a central venous catheter is placed for precise hemodynamic monitoring and administration of vasopressors to support his blood pressure. The chest X-ray is repeated, showing progression of the bilateral infiltrates, consistent with worsening pneumonia and possible acute respiratory distress syndrome (ARDS).

Further laboratory tests reveal a creatinine level that has risen to 2.0 mg/dL, raising concerns about acute kidney injury secondary to sepsis and hypoperfusion. The team initiates renal protective strategies and continues close monitoring of his renal function. This change in Mr. Thompson's status necessitates a reevaluation of his treatment goals and further interdisciplinary collaboration to optimize his care, with the team preparing for potential escalation to more advanced supportive therapies if necessary.

Section 4

As Mr. Thompson remains under intensive care, the medical team closely monitors his response to the interventions. Over the next 24 hours, there is a slight improvement in his hemodynamic status with the administration of vasopressors; his blood pressure stabilizes at 102/64 mmHg, although his heart rate continues to hover around 115 bpm. The mechanical ventilation is set to provide adequate oxygenation, with an FiO2 of 50% and PEEP of 10 cm H2O, managing to sustain an oxygen saturation of 92%. However, despite these measures, Mr. Thompson's renal function continues to decline. His creatinine level spikes to 3.2 mg/dL, and his urine output drops to less than 0.5 mL/kg/hr, indicating worsening acute kidney injury.

In light of these developments, the nephrology team is consulted to assess the need for renal replacement therapy. The decision is made to initiate continuous renal replacement therapy (CRRT) to manage the fluid overload and support renal function. Meanwhile, repeat blood cultures and sensitivity testing reveal that Mr. Thompson's pneumonia is caused by a highly resistant strain of Pseudomonas aeruginosa, necessitating a change in antibiotic regimen to a combination of ceftazidime-avibactam and amikacin to combat the resistant organism effectively.

The multidisciplinary team, including critical care, infectious disease, and nephrology specialists, collaborates to adjust the treatment plan. They emphasize the importance of maintaining adequate perfusion and oxygenation while addressing the infection and supporting renal function. The team also remains vigilant for signs of further complications, such as disseminated intravascular coagulation (DIC) or ongoing septic shock, and prepares to escalate care if needed. This comprehensive approach aims to stabilize Mr. Thompson further and prevent additional deterioration of his condition.

Section 5

As the team continues to manage Mr. Thompson's condition, they notice a change in his status over the next 48 hours. Although his hemodynamic parameters remain stable with the help of vasopressors, his oxygenation begins to show signs of deterioration. His oxygen saturation drops to 88% despite the FiO2 being increased to 60% on the ventilator, suggesting worsening respiratory function. Auscultation of his lungs reveals decreased breath sounds and crackles in both lower lobes, indicating possible progression of his pneumonia or development of acute respiratory distress syndrome (ARDS).

Concurrently, Mr. Thompson's lab results return with concerning findings. His platelet count has dropped to 90,000/µL, and his fibrinogen levels are low, raising suspicion for developing disseminated intravascular coagulation (DIC). The team also notes a slight increase in his bilirubin levels, now at 2.1 mg/dL, hinting at possible liver involvement, which could be secondary to his ongoing septic state. These changes prompt the team to enhance their focus on Mr. Thompson's coagulation status, considering the potential need for blood product support if DIC progresses.

In response to these new complications, the multidisciplinary team revisits the treatment strategy. The critical care team adjusts the ventilator settings to improve oxygenation, possibly considering prone positioning to enhance lung perfusion. The infectious disease specialists ensure the new antibiotic regimen is optimized for adequate dosing and coverage. Nephrology continues to monitor Mr. Thompson's response to CRRT closely, adjusting the parameters as needed to manage fluid balance and electrolyte disturbances. The team remains vigilant, recognizing that these developments require a delicate balance of interventions to stabilize Mr. Thompson while preventing further complications.