Case Study
A rapid response event was initiated by the bedside nurse for a patient who developed altered mentation and shallow breathing. On arrival of the condition team, the patient was found to be an 80-year-old female with a history of lung adenocarcinoma who presented a few hours ago for dyspnea on exertion and was found to have a large right-sided pleural effusion. Since admission, she had had progressive difficulty breathing, however, was awake and hemodynamically stable. The patient was planned for a thoracentesis under ultrasound guidance the following day.
Vital Signs
Temperature: 37.4 °F, axillaryBlood Pressure: 130/90 mmHg
Pulse: 120 beats per min – sinus tachycardia on the cardiac monitor
Respiratory Rate: 20 breaths per minPulse Oximetry: 75% on room air, 90% on 10 L high-flow nasal cannula
Focused Physical Examination
A quick exam showed an elderly cachectic female who appeared somnolent, not responsive to painful stimuli, using accessory muscles of respiration. No air entry was noted on the right lung field with dullness on percussion on auscultation. The remaining physical examination was unremarkable.
Interventions
On a quick review of the prior charted data, admission chest radiography, and the history of lung adenocarcinoma, the patient appeared to be in acute hypoxic respiratory failure because of massive pleural effusion. A cardiac monitor and pads were attached for hemodynamic monitoring. Due to hypoxemic respiratory failure, decreased mentation, and inability to protect the airway, the patient was initially ventilated via Ambu-bag and then emergently intubated using the rapid-sequence-intubation technique. Stat chest X-ray and arterial blood gas were obtained. Arterial blood gas showed pH 7.40, pCO 2 40 mmHg, pO 2 60 mmHg, spO 2 90%, which was significant for hypoxemia. Chest X-ray showed an increase in the effusion size compared to admission ( Fig. 29.1 ). Once the patient was stabilized, she was transferred to the intensive care unit for emergent thoracentesis.
Final diagnosis
Massive pleural effusion leading to acute hypoxic respiratory failure.
Massive Pleural Effusion
Pleural effusion is the build-up of excess fluid between the two layers of the pleura. The pleural space usually contains a small amount of pleural fluid, which is formed by pleural capillaries and drained through pleural lymphatics. This fluid helps in lubricating the pleural membranes and sliding motion between the two pleural layers during normal inspiratory and expiratory movements of the lung and chest wall. Pleural effusion accumulates if the pleural fluid formation is more than drainage or if the drainage is impeded in any way ( Table 29.1 for different causes of pleural effusion).
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Increased fluid production:
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Seen with increased intravascular hydrostatic pressure (as seen in heart failure), decreased colloid osmotic pressure (as seen in hypoproteinemia), or increased capillary permeability (seen in pneumonia or hypersensitivity reactions).
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Decreased rate of absorption:
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Seen in lymphatic obstruction (because of a tumor or decreased venous pressure) or reduced pressure in pleural space (seen in atelectasis)
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| Cause | Examples |
|---|---|
| Infectious |
|
| Malignant |
|
| Pulmonary |
|
| Cardiac |
|
| Gastrointestinal |
|
| Genitourinary |
|
Pleural fluid can be characterized as either transudate or exudate ( Table 29.2 ).
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Transudative:
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Results from imbalances in hydrostatic and oncotic pressures.
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Usually bilateral.
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In most cases, thoracentesis is not required as a diagnostic tool.
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Exudative:
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Results from pleural/lung inflammation, which increases capillary permeability or decreases lymphatic drainage.
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Exudative fluid is unilateral in most cases but can be bilateral.
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Thoracentesis is performed when the pleural fluid is suspected to be exudative.
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Light’s criteria: pleural fluid protein to serum protein ratio >0.5, pleural fluid lactate dehydrogenase (LDH) to serum LDH ratio >0.6, pleural fluid LDH greater than two-thirds times the upper limit of normal for serum LDH. If >1 of these criteria are met, then the pleural fluid is likely exudative.
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Pleural fluid acidosis (pH <7.30, normal 7.6) can be caused by increased acid production by pleural fluid cells, and bacteria or decreased hydrogen efflux from pleural space can also point toward an exudative effusion.
