Pulmonary edema is a pathophysiological entity characterized by the extravascular movement of fluid into the pulmonary interstitium and alveoli. The physiological determinants of pulmonary edema include (

Fig 1: Graphic representation of the physiological determinants involved in pulmonary edema.

1) hydrostatic pressure: which is described as the pressure within the capillaries that forces fluid out of the vessels

2) oncotic pressure; which is defined as the pressure related to blood proteins that helps retain fluid in the vessels

3) membrane permeability, which would be the ease with which fluid passes through capillary or alveolar walls.

Lymphatic channels are also important in maintaining fluid balance, as they allow the return of extravascular fluid to the central vasculature.

Pulmonary edema can be classified in different categories based on these physiological determinants of edema

Fig 2: Diagram showing the different categories of pulmonary edema according to physiological determinants.

• Hydrostatic pressure edema.
• Membrane permeability edema with or without diffuse alveolar damage (DAD).
• Mixed edema, which involves both increased hydrostatic pressure and increased membrane permeability.

The most common type is hydrostatic pressure edema, and its origin is usually cardiogenic due to left heart failure or volume overload. Differentiation at the onset of the condition between cardiogenic and noncardiogenic pulmonary edema is very important, since initial management differs depending on the cause, requiring in some cases, specific and urgent action (

Fig 3: Diagram on the differential diagnosis between cardiogenic edema and non-cardiogenic edema based on clinical and radiological findings.

There is a wide spectrum of etiologies of non-cardiogenic pulmonary edema including:

1- Acute respiratory distress syndrome (ARDS):

Increased capillary permeability that increases the movement of water, proteins and inflammatory substances from the intravascular space to the interstitial space and alveoli due to direct or indirect lung injury (sepsis, pancreatitis, etc.). Radiological findings on X-ray and CT can be summarized according to the stage of the disease, although some degree of overlap can be expected.

The progression of pulmonary edema in ARDS includes three phases: an acute phase (1–7 days) with proteinaceous edema and typically ventrodorsal density gradient opacities, a proliferative phase (8–14 days) marked by pneumocyte proliferation and stable radiologic findings, and a fibrotic phase (>15 days) that may result in resolution of the condition or pulmonary fibrosis, depending on the extent of injury and recovery. The phases are explained in more detail in

Fig 4: Diagram detailing the different phases of Acute respiratory distress syndrome (ARDS).

Clinical case 1:

Fig 5: A) Chest X-ray showing asymmetrical bilateral alveolar opacities predominating in the right lung (arrow) and B) Chest X-ray after 10 days, which shows a slight improvement in the opacities. orotracheal intubation tube (arrow) and jugular central ev catheter (asterisk).

Fig 6: Chest X-ray (A) showing improvement of consolidations, evidencing bilateral reticular opacities (asterisk) and cystic images (orange arrow) in the context suggestive of pneumatoceles. Lung CT: B) coronal reconstruction and C) axial sections. Ground-glass areas (orange asterisk) and images suggestive of ARDS with progression to fibrosis: distortion of the lung architecture, reticulation, traction bronchiectasis (red arrow) and pneumatoceles (orange arrow).

2- Neurogenic pulmonary edema:

Onset of pulmonary edema within minutes to hours after a neurological event (viral encephalitis, SAH, TBI, seizures, etc.) and resolution within 72 hours. This is a diagnosis of exclusion.

Pathophysiology: adrenergic response leading to increased hydrostatic pressure and pulmonary capillary permeability (mixed edema).

Clinical case 2:

Fig 7: A) and B) Axial cranial CT sections showing hematoma of the genu of the corpus callosum and blood contamination in the subarachnoid and chiasmatic cistern. C) Chest X-ray in AP showing bilateral perihilar consolidations (red asterisk) after aneurysm embolization D) Improvement of consolidations after 3 days. Orotracheal intubation tube (red arrow) and nasogastric tube ( green asterisk).

In the clinical context, when pulmonary edema appears after a neurological event (HSA + cerebral hematoma), we must think of neurogenic pulmonary edema.

3- Re-expansion pulmonary edema

This is a rare but potentially fatal iatrogenic complication that occurs following the rapid expansion of a collapsed lung after performing a thoracentesis for the treatment of pneumothorax or pleural effusion.

It involves both an increase in capillary permeability and hydrostatic pressure. The release of local and systemic inflammatory mediators leads to alterations in surfactant production and free radical-induced reperfusion injury. 

Risk factors for re-expansion pulmonary edema include:

 -High degree of lung collapse.

- prolonged duration of collapse (3 days).

- rapid lung re-expansion.

- high amount of air or fluid drained.

- negative pressure drainage.

- under 40 years of age.

Clinical case 3:

Fig 8: A) Chest X-ray showing a white left hemithorax due to hepatic hydrothorax and collapse of the underlying lung. Note the deviation of the trachea to the ipsilateral side (arrow). B) Chest X-ray after evacuation thoracentesis showing the pleural drainage tube (arrow) with resolution of the left pleural effusion and appearance of alveolar opacities in the left lung (yellow asterisk). C) Axial section and D) coronal reconstruction of a post-evacuation thoracic CT showing resolution of the left pleural effusion and a small amount of right pleural effusion (blue asterisk). Ground-glass and consolidative opacities (red asterisk) and septal thickening (arrow) are observed in the left lung, compatible with pulmonary edema due to re-expansion in the context.

When pulmonary edema appears after pleural cavity drainage, we must consider pulmonary edema due to re-expansion.

4- Negative pressure pulmonary edema-laryngospasm

This rare complication can occur after general anesthesia with intubation or with the use of a laryngeal mask, particularly in individuals with difficult intubation, young age, male sex, recent upper respiratory infections, obstructive sleep apnea (OSA), or a history of reactive airway disease. The condition is transient and reversible if recognized and managed appropriately, often presenting with pink, foamy sputum.

It is caused by the transmission of intrapleural negative pressure in the pulmonary capillary bed

Fig 9: Sequence of events of pulmonary edema secondary to laryngospasm. Source: Carrillo Esper R, Ortiz Montaño Y, Peña Pérez CA. Post-extubation acute pulmonary edema secondary to laryngospasm. Rev Mex Anest 2012;35(3):200-202.

Clinical case 4:

Fig 10: A) Chest X-ray in the immediate postoperative period showing bilateral diffuse alveolar infiltrates (asterisk) compatible in the clinical context with negative pressure pulmonary edema. B) Chest X-ray showing resolution of alveolar opacities at 72 hours.

The presence of acute pulmonary edema after surgery (after general anesthesia with intubation or laryngeal mask) may raise suspicion of laryngospasm/negative pressure edema.

5- Pulmonary veno-occlusive disease (PVOD).

This is a rare and potentially serious cause of group 1 pulmonary hypertension. Unlike most entities in this group (which present arterial involvement), it produces extensive venous and capillary involvement.

Differentiating PVOD from primary pulmonary hypertension is essential, as vasodilatory therapies can cause fulminant acute pulmonary edema. 

The condition is characterized by an aberrant response to endothelial injury that leads to generalized fibrosis of the venous system.

Clinical case 5:

Fig 11: A) Axial CT section of the chest in the soft tissue window showing an increase in the size of the pulmonary artery trunk (TP: 36 mm), suggestive of pulmonary hypertension. B) Axial CT section of the chest showing increased mediastinal lymphadenopathy (arrowhead). C) Axial CT section with enlargement of the chest in the pulmonary window showing bilateral and diffuse involvement in the form of multiple poorly defined centrolobular nodules (orange arrow) and septal thickening (pink arrow).

In patients with pulmonary PH, the presence of ground-glass opacities (centrilobular distribution), septal lines and lymphadenopathy are indicative of pulmonary veno-occlusive disease, usually in the context of scleroderma or after administration of CT.

6- Systemic capillary leak syndrome (SCLS)

It’s a rare condition characterized by sudden and reversible capillary hyperpermeability, leading to rapid plasma extravasation from the intravascular space into the interstitial space. It presents with a triad of symptoms: shock due to vascular collapse, hemoconcentration, and hypoalbuminemia. 

SCLS is commonly triggered by infections or chemotherapy and is associated with monoclonal gammopathy of uncertain significance.

Clinical case 6:

Fig 12: A) Axial CT section of the chest in the pulmonary window showing septal thickening (→) and bilateral ground-glass involvement (orange asterisk), findings compatible with acute pulmonary edema. B) Axial CT section of the chest in the mediastinal window showing bilateral pleural effusion predominantly on the right (green asterisk). C) Axial CT section of the abdomen showing soft tissue edema and mesenteric edema (red asterisk).

Findings of acute pulmonary edema in the unique combination of hypotension, hemoconcentration, and hypoalbuminemia should lead to SCLS.

7- Transfusion-related acute lung injury (TRALI)

It is a rare complication that can occur immediately or up to 6 hours after transfusion of blood products.

It is characterized by alveolar and interstitial infiltrates + septal thickening + pleural effusion that usually disappear within 4 days.

The pathophysiology of TRALI is not fully understood, but it may involve an inflammatory reaction mediated by antibodies against leukocyte or antigranulocyte antigens present in transfused blood.

Clinical case 7:

Fig 13: A) Chest X-ray showing extensive bilateral alveolar opacities (orange asterisk) 3 hours after red blood cell transfusion, suggestive in the clinical context of pulmonary edema due to TRALI. The left peritoneal drainage in the splenectomy surgical bed is also observed (green arrow). B) The patient is subsequently intubated, admitted to the Intensive Care Units (ICU), and the study is completed with a chest CT that confirms diffuse bilateral alveolar involvement (orange arrow). A left pleural effusion is also observed (green asterisk), probably reactive to the recent splenectomy. C) Chest X-ray after 5 days showing a clear improvement of the bilateral pulmonary edema.

When faced with acute pulmonary edema after transfusion, transfusion-related acute lung injury (TRALI) should be considered.

8- Pulmonary edema due to near-drowning

It can develop after near-drowning, either in salt or freshwater. The condition typically presents with localized, perihilar, or diffuse pulmonary opacities on radiological imaging. It generally develops within the first 8 hours and resolves within the first week. The pathophysiology involves the destruction of surfactant and alteration of the alveolar-capillary membrane, which increases permeability and leads to pulmonary edema.

Clinical case 8:

Fig 14: A) Chest X-ray showing bilateral alveolar pulmonary opacities (pink asterisk). B), C) and D) Axial CT sections of the chest in the pulmonary window showing extensive bilateral ground-glass parenchymal involvement (pink asterisk), thickening of the interlobular septa and more consolidated opacities in the lower lobes (green asterisk) with the air bronchogram sign (red arrow). The findings are attributable to pulmonary edema related to ARDS due to near-drowning.

When localized, perihilar, or diffuse pulmonary opacities are present in a nearly drowned patient, we must consider pulmonary edema due to near-drowning. 

9- Focal pulmonary edema due to pulmonary thromboembolism

Focal pulmonary edema is a rare complication of pulmonary embolism, which can occur independently of pre-existing cardiopulmonary disease. 

The pathophysiology behind this phenomenon is still not fully understood, but it is thought to result from "hyperperfusion" in areas of the lung unaffected by the embolism or the release of inflammatory mediators that cause edema in hypoperfused areas.

Clinical case 9:

Fig 15: A) Coronal section of thoracic CT angiography in soft tissue window showing signs of pulmonary thromboembolism with filling defects of the main pulmonary arteries with bilateral lobar and segmental extension (red arrow). Contrast reflux into the inferior vena cava indicative of right heart overload (red asterisk). B) and C) Coronal sections of thoracic CT angiography in pulmonary window showing ground-glass and consolidative alveolar opacities in middle lobe and right upper lobe, with central perihilar and peripheral distribution (yellow asterisk), which in the context, without other accompanying symptoms, may suggest focal pulmonary edema.

In rare cases, pulmonary edema may be focal in PE (clinical conditions may allow us to rule out other more frequent causes of opacities such as infection).

Other entities:

10- Pulmonary Edema Due to Altitude: Occurs after rapid ascent to altitudes greater than 3000 meters. The pathophysiology involves altered permeability of the alveolar-capillary barrier without alveolar damage, leading to endothelial leak due to hypoxic pulmonary vasoconstriction and high capillary pressure.

11- Post-Pneumonectomy Pulmonary Edema: Can occur between 24 and 48 hours after pneumonectomy, primarily related to excessive fluid intake during surgery.

12- Opioid-Induced Pulmonary Edema:Considered in patients with opioid overdose and significant hypoxia within the first 24 hours post-overdose.

In summary, identifying the underlying etiology of edema is crucial to establishing appropriate treatment.