A young male with dyspnoea after placement of a pleural drain

A 20-year-old man presented to the emergency room (ER) with a 3-day history of chest pain and breathlessness. He was asymptomatic 3 days earlier when he had sudden onset of left-sided chest pain. It was associated with breathlessness on minimal exertion. There was no history of fever, cough, or wheezing. Upon arrival in the ER, his pulse rate was 120/minute, blood pressure was 100/60 mmHg, respiratory rate was 30/minute with the use of accessory muscles of respiration, and SpO₂ was 85% on room air. Clinical examination revealed absent breath sounds over the left side of the chest with a tympanic note on percussion. He was started on oxygen, and an emergent chest X-ray revealed tension pneumothorax (Fig. 1a). A pigtail catheter was placed into the left pleural cavity immediately. The patient experienced immediate symptom relief. However, after 30 minutes, he developed a severe cough and worsening breathlessness. His oxygen requirement increased from 2 to 8 L/minute. His chest X-ray was repeated, which showed non-homogeneous opacities on the left side with expansion of the collapsed lung (Fig. 1b). The clinical and radiological features were suggestive of re-expansion pulmonary oedema (REPE).

Close

FIG 1. (a) Chest X-ray (posteroanterior view) showing hyperlucent left hemithorax with absent lung markings and downward displacement of diaphragm, suggesting tension pneumothorax and (b) after placement of pigtail catheter in the left pleural cavity showing heterogeneous opacities in the left hemithorax

Export to PPT

REPE can occur when a collapsed lung rapidly expands following the evacuation of a large volume of air or fluid.^1,2 It is a potentially fatal condition and has a mortality of around 20%.^1-3 The exact mechanism is not known, but it appears to occur due to increased leakiness of the pulmonary vasculature.¹ Various hypotheses that have been proposed include a reperfusion-induced inflammatory response with the formation of free radicals, altered lymphatic clearance, and an increase in venous return to the lung, causing increased hydrostatic pressure.³ The mechanism of REPE is thought to be due to damage to the pulmonary interstitium (PI) and an imbalance of hydrostatic forces. The PI is bordered by visceral pleura and forms a barrier between the alveoli and the capillaries. Changes in intrapleural pressure directly affect the interstitium. Rapid re-expansion of the underlying collapsed lung causes pressure-related mechanical damage to the pulmonary vasculature, leading to increased permeability. The sudden reversal of hypoxic vasoconstriction is proinflammatory, which precipitates oxidative stress and fluid production. When this is combined with increased negative intrapleural pressures resulting from the removal of large volumes of air or fluid, there is a sudden reduction in interstitial pressure, which creates an increased gradient for fluid movement across the alveolar-capillary barrier, leading to REPE.⁴ Persistent cough is the earliest indicator and should be considered as a sign to stop further drainage immediately.³ Radiographic changes, such as ipsilateral infiltrates after drainage of pleural fluid or air, should aid in diagnosis. Management is supportive until symptoms such as cough or breathlessness improve. The use of oxygen, bilevel positive pressure ventilation (BiPAP), invasive mechanical ventilation, and haemodynamic support has been described in the literature.⁴

Our patient was managed with BiPAP for a day, followed by oxygen with a face mask. Over the next 2 days, he was taken off oxygen and showed complete radiological clearance.