pneumothorax - Nursing Case Study

Pathophysiology

• Primary mechanism: Air enters the pleural space between the lung and chest wall, disrupting the negative pressure that normally keeps the lung expanded. This leads to partial or complete lung collapse, impairing gas exchange and causing respiratory distress.

• Secondary mechanism: The entry of air can occur from a breach in the lung surface (spontaneous pneumothorax) or from trauma (traumatic pneumothorax), leading to increased intrapleural pressure. This pressure imbalance reduces lung volume and compromises ventilation.

• Key complication: If the air continues to accumulate, it can cause a tension pneumothorax, where the pressure in the pleural space exceeds atmospheric pressure, compressing the heart and other mediastinal structures, potentially leading to cardiovascular instability and requiring immediate intervention.

Patient Profile

Demographics:

35-year-old male, construction worker

History:

• Key past medical history: History of asthma, smoker for 10 years

• Current medications: Albuterol inhaler as needed, occasional ibuprofen for pain

• Allergies: Penicillin

Current Presentation:

• Chief complaint: Sudden onset of sharp chest pain and difficulty breathing

• Key symptoms: Shortness of breath, chest tightness, dry cough, fatigue

• Vital signs: Blood pressure 95/60 mmHg, heart rate 110 bpm, respiratory rate 28 breaths per minute, oxygen saturation 88% on room air, temperature 37.2°C (99°F)

Section 1

As the medical team continues to assess the 35-year-old male construction worker, they observe a further decline in his respiratory status. Despite the administration of supplemental oxygen via nasal cannula, his oxygen saturation remains at a concerning 85%. The patient is visibly distressed, demonstrating accessory muscle use and an increased respiratory rate of 32 breaths per minute. A repeat auscultation of his chest reveals diminished breath sounds on the right side, with an increased resonance upon percussion, suggesting an expanding pneumothorax.

Shortly thereafter, a STAT chest X-ray confirms the presence of a large right-sided pneumothorax, now showing signs of shifting of the mediastinum towards the left, indicating the development of a tension pneumothorax. The patient's blood pressure has dropped further to 90/55 mmHg, and his heart rate has increased to 120 bpm, reflecting compromised cardiac output due to the increased intrathoracic pressure. These findings necessitate immediate intervention to prevent further hemodynamic instability.

The clinical team quickly decides to perform a needle decompression followed by chest tube insertion to relieve the pressure in the pleural space. After the procedures, the patient's oxygen saturation begins to improve, and his breath sounds become more audible on the affected side. However, the patient remains tachycardic, and his blood pressure is only marginally better, indicating potential ongoing complications such as re-expansion pulmonary edema or an underlying persistent air leak that would require further monitoring and management. This scenario emphasizes the need for vigilant observation and the potential for additional interventions to stabilize the patient fully.

Section 2

Following the initial interventions, the medical team continues to closely monitor the patient for any new complications. Over the next few hours, the patient's respiratory status stabilizes, with oxygen saturation improving to 92% on supplemental oxygen via face mask. However, despite these improvements, the patient continues to exhibit tachycardia, with heart rates consistently ranging between 110-115 bpm, and his blood pressure remains at a low 95/60 mmHg. These signs prompt the team to consider the possibility of re-expansion pulmonary edema or a persistent air leak, which could account for the ongoing cardiovascular instability.

To further investigate, a repeat chest X-ray is ordered, which reveals a slight opacification in the right lower lung field suggestive of re-expansion pulmonary edema. Additionally, an air leak is detected in the chest tube drainage system, raising concerns about the integrity of the lung re-expansion process. Laboratory tests show a mild leukocytosis with a white blood cell count of 12,500/mm³ and a slight elevation in lactate levels at 2.5 mmol/L, indicating a moderate stress response and potential hypoperfusion.

Given these findings, the clinical team decides to adjust the patient's management plan. Diuretics are considered to manage the suspected pulmonary edema, and the chest tube is inspected for proper positioning and function to address the air leak. The patient is also kept on continuous cardiac monitoring and receives intravenous fluids cautiously to maintain adequate perfusion without exacerbating the pulmonary edema. This approach requires careful balancing to avoid further complications while ensuring that the patient's respiratory and cardiovascular status stabilizes. The team remains vigilant, anticipating further diagnostic evaluations and interventions as necessary to guide the patient safely through his recovery journey.

Section 3

As the clinical team continues to navigate the complexities of the patient's condition, they focus on the new diagnostic results that could illuminate the path forward. The repeat chest X-ray findings of opacification in the right lower lung field suggestive of re-expansion pulmonary edema prompt a series of targeted assessments. The team observes the patient's respiratory effort, noting mild dyspnea with occasional use of accessory muscles, but no significant cyanosis. Auscultation reveals diminished breath sounds in the right lower lobe, consistent with the X-ray findings, but no crackles are detected, which might indicate worsening edema.

Meanwhile, the air leak detected in the chest tube system necessitates immediate attention. Upon close inspection, it is confirmed that the leak is persistent, and thus, the team assesses the position of the chest tube, ensuring it is not kinked or displaced. They decide to apply additional suction to the chest tube to facilitate re-expansion and alleviate the air leak, while monitoring for any signs of increased respiratory distress or hemodynamic instability that could suggest a tension pneumothorax.

In parallel, laboratory results continue to provide insight into the patient’s condition. The mild leukocytosis and elevated lactate levels suggest an ongoing inflammatory response and potential tissue hypoperfusion. These findings, combined with the patient’s persistent tachycardia and hypotension, underscore the need for judicious management of intravenous fluids. The team opts to administer a low-dose diuretic cautiously, aiming to mitigate the pulmonary edema without compromising blood pressure further. Throughout this process, the clinical team remains vigilant, ready to adapt their strategy as the patient's response to these interventions unfolds, thus ensuring a balanced approach to this complex clinical scenario.

Section 4

As the clinical team continues to monitor the patient closely, new diagnostic results reveal a slight increase in the size of the pneumothorax on the right side, as evidenced by a follow-up chest X-ray. This finding raises concerns about the effectiveness of the current chest tube management and prompts the team to reassess the patient's treatment plan. Concurrently, arterial blood gas analysis shows worsening respiratory acidosis, with a pH of 7.30, partial pressure of carbon dioxide (PaCO2) at 52 mmHg, and partial pressure of oxygen (PaO2) at 68 mmHg. These results indicate inadequate gas exchange and a potential need for enhanced respiratory support.

In response to these developments, the clinical team re-evaluates the patient's respiratory status, noting an increase in respiratory rate to 28 breaths per minute and continued use of accessory muscles, suggesting escalating respiratory distress. The heart rate remains elevated at 110 beats per minute, and blood pressure is 92/60 mmHg, indicative of persistent hemodynamic instability. Given these changes, the team decides to increase the supplemental oxygen delivery and prepares for potential escalation to non-invasive ventilation to improve alveolar ventilation and address the respiratory acidosis.

Despite these interventions, the patient begins to exhibit signs of confusion and agitation, raising concerns about potential cerebral hypoxia or increasing carbon dioxide levels. The team urgently reviews the patient's neurological status, considering the need for further imaging to rule out other causes of neurological compromise. As they prepare for a potential transfer to the intensive care unit, the clinical team remains focused on balancing fluid management to avoid exacerbating the re-expansion pulmonary edema while optimizing respiratory and hemodynamic support. This dynamic situation requires careful consideration of priorities and constant adjustment of the treatment strategy, underscoring the complexity of managing patients with pneumothorax and associated complications.

Section 5

New Complications:

As the clinical team continues to manage the evolving situation, a new complication arises: the patient develops signs consistent with re-expansion pulmonary edema, a known risk following rapid re-expansion of a collapsed lung. The patient begins to exhibit increased crackles upon auscultation of the right lung, and oxygen saturation levels drop to 85% despite high-flow oxygen therapy. The patient's respiratory distress intensifies, with a respiratory rate climbing to 32 breaths per minute and pronounced intercostal retractions.

In response to these alarming developments, the team urgently reassesses the fluid management strategy, recognizing that careful adjustment is crucial to prevent further exacerbation of pulmonary edema. Intravenous fluids are cautiously reduced, and diuretics are considered to manage fluid overload. Meanwhile, the patient's blood pressure has dropped further to 88/58 mmHg, compounding the challenge of maintaining adequate perfusion without worsening the pulmonary condition. Close monitoring of urine output and electrolytes becomes imperative to guide fluid and electrolyte management effectively.

Faced with these complications, the clinical team decides to initiate non-invasive positive pressure ventilation (NIPPV) to support the patient's breathing effort and improve alveolar recruitment, while minimizing the risk of intubation-related complications. This intervention aims to enhance gas exchange, address the respiratory acidosis, and reduce the work of breathing. The team prepares to transfer the patient to the intensive care unit for closer monitoring and advanced respiratory support, understanding that the management of pneumothorax with concurrent re-expansion pulmonary edema requires vigilant observation and timely adjustments to the treatment plan. This scenario underscores the complexity and dynamic nature of critical care management, where rapid clinical reasoning and coordinated team efforts are essential to navigate the patient's deteriorating condition.