Last Updated on April 10, 2019
Reexpansion pulmonary edema is a non-cardiogenic pulmonary edema that occurs in the setting of rapid expansion of a collapsed lung. It results in acute onset shortness of breath that usually results within hours of re-expansion but can be delayed by 24 hours in some cases. It occurs following approximately 1% of pneumothorax re-expansions or thoracentesis procedures.
Reexpansion Pulmonary edema may be considered an iatrogenic complication due to rapid emptying of the pleural cavity.
Although most patients completely recover within five to seven days, severe re-expansion pulmonary edema can lead to sequestration of large quantities of fluid in the lung, which may result in shock and possibly death.
Re-expansion pulmonary edema is infrequent but death may occur in up to 20% of the cases.
The incidence of occurrence is about 1%.
Pathophysiology of Reexpansion Pulmonary Edema
The pathophysiology of re-expansion pulmonary edema is multifactorial and not yet completely understood.
The main hypothesis considers it to be a result of an acute inflammatory response that causes damage to the alveolar–capillary membrane, and changes in the pulmonary lymphatic vessels and in the surfactant.
Another theory suggests increased permeability of the pulmonary capillaries as a result of inflammation.
Still another theory suggests increased pulmonary hydrostatic pressure and pressure-induced mechanical disruption of the alveolar capillaries to be responsible.
Risk factors
Rapid lung re-expansion in the following settings
- Large pneumothorax
- Young patients [age between 20 and 40 years]
- If lung has been collapsed for over 7 days
- Application of high negative pressures during thoracic drainage (> 20 cm H2O)
- Rapid lung expansion with drainage of large volumes of pleural fluid (> 1.5 L).
Clinical features of Reexpansion Pulmonary Edema
The extent of edema defines the clinical picture varies according to the extent of the edema.
64% of patients are symptomatic during the first hour after the puncture.
Suggestive symptoms are
- Persistent cough
- Tachycardia
- Tachypnea
- Hypoxemia
- Hemodynamic instability.
- Chest discomfort
The cardinal signs are tachypnea, tachycardia, and crackles on the affected side of the lung as well as hypoxemia, which may be refractory to oxygen therapy.
Imaging
X-ray
A chest radiograph is usually diagnostic. It shows unilateral alveolar (air-space) opacity
CT
CT of ground glass opacification [area of increased attenuation in the lung on computed tomography ].
It may be peripheral in distribution and associated with smooth interstitial thickening.
Treatment of Reexpansion Pulmonary Edema
Management is generally supportive and varies by severity of the condition.
Oxygen supplementation may prove adequate in patients with mild symptoms.
Patients with severe symptoms require endotracheal intubation and mechanical ventilation.
Lateral decubitus on the affected side is recommended. [Having the patient lie on his or her unaffected side] is therapeutic.
Diuretics, bronchodilators, prostaglandin analogues and NSAIDs have been used but the evidence is not clear about their use.
Prevention
Following strategies may help
- Use of low negative pressure (< −20 cm H2O) for suction during tube thoracostomy
- Limiting drainage to about 1 to 1.5 L of pleural fluid.
- Drainage catheters can be intermittently plugged to prevent rapid lung re-expansion.
References
- Sherman SC. Reexpansion pulmonary edema: a case report and a review of the current literature. J Emerg Med. 2003;24:23–7. 10.1016/S0736‐4679(02)00663‐7
- Jaber S, Perrigault PF, Souche B, Pouzeratte Y. Re‐expansion pulmonary edema with normal pulmonary artery occlusion pressure during liver transplantation. Intensive Care Med. 2002;28:376. 10.1007/s00134‐001‐1195‐0
- Sue R, Matthay MA, Ware LB. Hydrostatic mechanisms may contribute to the pathogenesis of human re‐expansion pulmonary edema. Intens Care Med. 2004;30:1921–6. 10.1007/s00134‐004‐2379‐1
- Feller‐Kopman D, Walkey A, Berkowit D, Ernst A. The relationship of pleural pressure to symptom development during therapeutic thoracentesis. Chest. 2006;129:1556–60. 10.1378/chest.129.6.1556