First described in 1958 by Carlson et al. , vacuo pulmonary edema or reexpansion pulmonary edema is a complication of reexpansion of the lung parenchyma after collapse, whether related to liquid effusion [2,3] or gaseous effusion from the pleura [4,5]. Early diagnosis based on both clinical and radiological evidence allows for prompt and effective treatment. We report the case of a 33-year-old patient with reexpansion pulmonary edema after drainage of a spontaneous pneumothorax.
Patient and Observation
A 33-year-old patient, a 12 pack/year smoker with no specific medical/surgical history who had been admitted to the emergency department for right chest pain, associated with dry cough and moderate dyspnea evolving for three days. On physical examination, the patient had a regular pulse, was normotensive, and had a pulse oxygen saturation of 95% with pleuropulmonary examination of a gaseous pleural effusion syndrome of the right hemithorax. Electrocardiography showed no evidence of myocardial ischemia. The initial chest X-ray (Figure 1) showed a right pneumothorax of moderate size, for which a thoracic drainage with a Joly drain was performed. The evolution after drainage was marked by a brief resolution of the symptoms before the reappearance one hour later of severe dyspnea and the occurrence of an incoercible cough requiring a thoracic CT scan.
The CT scan (Figure 2) showed: ground glass areas associated with scattered condensation foci in the right lung hemifield with a right apical paraseptal and centrolobular emphysema bulla.
The treatment consisted of hemodynamic rebalancing with oxygen therapy associated with rest and monitoring. The patient's evolution was uneventful.
Vacuo pulmonary edema or reexpansion edema is a rare complication, most often affecting the lung on the drained side such as in our patient, but which can be bilateral or contralateral .
Its real frequency is unknown. However, an incidence varying from 0.9% to 29.8% is reported in the literature .
The pathophysiology of vacuo pulmonary edema is complex and not fully understood. However, the alteration of the permeability of the alveolar-capillary membrane is the element incriminated by all studies . This alteration is secondary to a decrease in surfactant activity, mechanical distension of the endothelial pores when ventilation of the collapsed lung is restored and excessive production of oxygen free radicals that are toxic to the alveolar-capillary membrane.
A subset of patients with spontaneous pneumothorax appears to be at increased risk of developing vacuo pulmonary edema . These risk factors are the young age of the patient as in our case, diabetes, the size of the pneumothorax, the duration of collapse or associated symptoms and the drainage techniques.
Clinically vacuo pulmonary edema can manifest itself in 3 forms :
- The asymptomatic form: of purely radiological discovery.
- The minor form: the clinical picture is summarized by a cough, mild dyspnea and sometimes minimal foamy sputum. The evolution is benign.
- The severe form: is manifested by intense dyspnea, incoercible cough, abundant sputum, serous, frothy, cyanosis and hypotension sometimes severe, real cardiovascular collapse with oligo-anuria, whose evolution could be fatal with a mortality rate between 15 to 20%. In the specific case of our patient, the clinical signs found: severe dyspnea and incoercible cough, are similar to those described in this form.
The diagnosis of pulmonary reexpansion edema is radioclinical. Chest radiography, although not specific, ensures the diagnosis by showing a unilateral alveolar syndrome. Chest CT shows ground-glass areas interspersed with parenchymal condensation, interlobular septal thickening, and intralobular interstitial thickening [10,11].
The treatment of reexpansion pulmonary edema relies above all on prevention . All authors agree on the necessity not to set up suction, limiting oneself to a simple siphoning on a water valve jar; in our case this measure was not sufficient; it also seems interesting to control the air outlet by intermittent clamping of the drain. Symptomatic treatment is based on rest and monitoring in asymptomatic forms associated with oxygen therapy in minor forms. Severe forms require in addition hemodynamic rebalancing and sometimes even the use of assisted ventilation. There is no consensus on the use of diuretics, corticoids and colloid agents [9,12].
Although rare the possibility of re-expansion pulmonary edema should always be present in the minds of physicians involved in the management of a pleural effusion. Identification of a patient at risk, early detection of clinical and radiological manifestations, and initiation of appropriate treatment can reduce the effects of this complication.
Conflicts of Interest
We declare not to have any conflicts.