Teaching Case

A 27 year old, tall and thin, healthy man, with no underlying lung disease, came to the hospital complaining of right-sided pleurodynia lasting for 2 weeks, without remembering acute onset of the
pain and the patient was generally in a good condition.

After medical examination, the only pathological finding, was a decrease of vesicular murmur of the right lung. Chest x-ray demonstrated a large right-sided pneumothorax. Laboratory tests were normal
(Fig. 1,2). He was then admitted immediately to the surgery room where a drainage catheter 40 F was inserted and a negative pressure was applied. A chest x-ray, 35 minutes later, showed complete
re-expansion of the right lung with diffuse bronchoalveolar infiltrations (Fig. 3). He was then symptomatic with acute dry cough, right pleurodynia and dyspnea, but he was hemodinamically stable. A
chest x-ray 24 hours later revealed complete remission of pulmonary infiltrations (Fig 4).

Predisposing factors for re-expansion pulmonary edema are: 1) Prolonged duration of pneumothorax, 2) Large pneumothorax, 3) Young age (<40) and 4) Quick
re-expansion of the collapsed lung. 64% of the cases occur within the first hour after re-expansion and the remaining 36% within 24 hours. REPE may progress for 24-48 hours and may persist for 4-5 days,
but it usually resolves within the first week. Although REPE involves the whole re-expanded lung, there are cases involving both lungs or a lobe of the ipsilateral lung.
The seriousness of the situation varies from asymptomatic to lethal cardiopulmonary insufficiency in 20% of the cases. Clinically it may present with dyspnea, tachypnea, tachycardia, central
cyanosis, pleurodynia, hypotension, nausea, vomiting and dry or productive cough with frothy pink sputum.
Albumin concentration in the sputum of patients with REPE is high, approximating the levels of serum albumin, implying that the fluid of pulmonary oedema is exudate. The pathophysiological
mechanisms explaining REPE are:
1) Chronic hypoxia of the pulmonary capillaries, which causes pulmonary microvascular injury and increased permeability. This has been shown from studies in rabbits, which revealed increased
concentration of pro-inflammatory cytokines (TNF, IL-1) in the pulmonary oedema fluid. Free radical generation (OH, H2O2) during re-expansion and reoxygenation of the collapsed lung contributes to
the endothelial cell injury and increased permeability .
2) Loss and decreased production of surfactant.
3) Increased cardiac output after re-expansion of the chronically collapsed lung, which elevates hydrostatic pressure of the pulmonary capillaries.
4) Changes in lymphatic flow of the lungs.
Other conditions with rapid re-expansion of one lung may be complicated with REPE. These include evacuating thoracocentesis of big pleural effusion, removal of large mediastinal or intrathoracic
mass, repair of diaphragmatic hernia, removal of intrathoracic haematoma, removal of a huge intra-abdominal tumor and after one lung ventilation.