18th February 2025

Non-cardiogenic pulmonary oedema

Overview of non-cardiogenic pulmonary oedema

This describes alveolar fluid accumulation which is not secondary to increased pulmonary capillary pressure (pulmonary artery wedge pressure ≤18 mmHg in pulmonary artery or Swan-Ganz right heart catheter study).

Acute respiratory distress syndrome

Acute respiratory distress syndrome (ARDS) is an important cause of non-cardiogenic pulmonary oedema. It can result from sepsis, pneumonia, massive trauma with shock, DIC, acute pancreatitis, and inhalation of vomit, smoke or toxic chemicals.

Diagnostic (Berlin) criteria are as follows:

• Timing: onset of lung injury within 1 week of insult or new/worsening respiratory symptoms over a week
• Imaging: bilateral opacities on CXR not fully explained by effusions, collapse or nodules
• Origin of oedema: respiratory failure not fully explained by cardiac failure or fluid overload
• Oxygenation: hypoxaemia (PaO2/FiO2 ratio ≤ 300 requiring a minimum PEEP/CPAP of 5 cmH2O to maintain target sats)

Management is with respiratory support (often in ITU) and treatment of underlying causes. CPAP may be adequate in the first instance but a majority of patients will need intubation and ventilation.

High altitude pulmonary oedema

High altitude pulmonary oedema (HAPE) occurs after rapid ascent to altitudes above 2500-3000 m and typically occurs 2-5 days after the ascent. It is the most common cause of death in high altitude sickness, with a mortality rate of more than 10% when treated and 50% when untreated. This is thought to occur due to reduced environmental FiO2 at higher altitudes, which leads to uneven hypoxia-driven vasoconstriction to physiologically address ventilation-perfusion mismatch. This increases vascular resistance in the pulmonary arteries, causing pulmonary hypertension. Increased hydrostatic pressure leads to capillary leak and pulmonary oedema.

Symptoms include breathlessness (particularly reduced exercise tolerance), cough and chest tightness. Acute altitude sickness and cerebral oedema may occur at the same time.

Risk factors include: male sex, prior high altitude pulmonary oedema, fast ascent rate, high peak altitude, cold exposure, high intensity of exertion, pre-existing pulmonary hypertension and genetic factors.

The most important management strategy is to descend until there is resolution of symptoms. Oxygen may be a temporising measure if descent is delayed. Nifedipine and phosphodiesterase inhibitors may be used as adjuncts.

Other causes of non-cardiogenic pulmonary oedema

• Transfusion-related acute lung injury (TRALI) – pulmonary oedema and hypoxia within 6 hours of a blood transfusion. It can be associated with fever and usually causes hypotension compared to transfusion-associated circulatory overload (TACO), with which there is often hypertension. Troponin and NT-pro-BNP are not usually raised, but the latter may be.
• Re-expansion pulmonary oedema – occurs after rapid expansion of a collapsed lung, e.g. after large volume pleural tap or drainage (greater than 1-1.5 L) with acute shortness of breath usually occurring within hours. It is self-limiting and usually requires only supportive management.
• Neurogenic pulmonary oedema – may be precipitated by epileptic seizures, traumatic brain injury or intracranial haemorrhage. Symptom onset is usually within minutes to hours and resolves after 48-72 h.
• Post-obstructive (e.g. after upper airway obstruction due to foreign object or hanging) pulmonary oedema – occurs due to increasing negative intrathoracic pressure whilst trying to inspire despite upper airway obstruction, which substantially increases venous return and may cause vascular damage
• Salicylate toxicity and opioid overdose
• Hypoalbuminemia is not a cause of pulmonary oedema but carries a worse prognosis when present

References

• Colucci WS. Treatment of acute decompensated heart failure: Specific therapies. [Internet]. Gottlieb SS, Hoekstra J, Dardas TF, editors. UpToDate. 2022 [cited January 30 2022]. Available from: https://www.uptodate.com/contents/treatment-of-acute-decompensated-heart-failure-specific-therapies
• Garan AR. Pathophysiology of cardiogenic pulmonary edema. [Internet]. Colucci WS, Dardas TF, editors. UpToDate. 2022 [cited January 30 2022]. Available from: https://www.uptodate.com/contents/pathophysiology-of-cardiogenic-pulmonary-edema 
• Tidy C, Jackson C. Acute Pulmonary Oedema. [Internet]. Patient.info. 2018 [cited January 30 2022]. Available from: https://patient.info/doctor/acute-pulmonary-oedema 
• Henson VL, Kendall JM, Burrows L, Kilgour P. Cardiogenic Pulmonary Oedema. [Internet]. Royal College of Emergency Medicine. 2021 [cited January 30 2022]. Available from: https://www.rcemlearning.co.uk/reference/cardiogenic-pulmonary-oedema
• Knott L, Bonsall A. Acute (Adult) Respiratory Distress Syndrome. [Internet]. Patient.info. 2019 [cited June 01 2022]. Available from: https://patient.info/doctor/acute-adult-respiratory-distress-syndrome
• Givertz M. Noncardiogenic pulmonary edema [Internet]. Gottlieb S, Finlay G, editors. UpToDate. 2021 [cited June 01 2022]. Available from: https://www.uptodate.com/contents/noncardiogenic-pulmonary-edema
• Auerbach, Paul S. (2017). Wilderness Medicine. Elsevier. pp. 20–25