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Pulmonary oedema 

Pulmonary oedema

Pulmonary oedema

Nicholas W. Morrell

and John D. Firth



This chapter has been retired and will not be updated further. The subject matter of this chapter is to be found in Chapter 16.15.1 of this online update.

Updated on 29 Oct 2015. The previous version of this content can be found here.
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date: 24 April 2017

The formation of pulmonary oedema depends on the balance between capillary hydrostatic pressure, interstitial tissue pressure, plasma colloid osmotic pressure, endothelial permeability, and lymphatic function. The efficiency of lymphatic drainage of interstitial fluid (which can increase >10-fold) is critical in determining the onset and extent of hydrostatic oedema.

Pulmonary capillary pressures in the range 25 to 35 mmHg increase the filtration of water and small solutes; interstitial oedema and pleural effusions result. Pulmonary capillary pressures greater than 35 mmHg cause blood and gas barrier disruption (stress failure); protein-rich fluid and red cells fill the air spaces. Endothelial disruption leads to oedema fluid with a high protein content and activation of coagulation, predisposing towards interstitial fibrosis. The dangerous combination of hydrostatic and high-permeability pulmonary oedema (which is slower to resolve) occurs in neurogenic and high-altitude pulmonary oedema.

Clinical features—the characteristic symptom of pulmonary oedema is breathlessness, which comes on more or less acutely in the first instance. Orthopnoea and paroxysmal nocturnal dyspnoea develop later because of postural hydrostatic factors. Typical physical signs are of diminished breath sounds and fine lung crepitations at the bases, but in the most dramatic cases the patient produces pink, frothy fluid from their mouth and looks as though they are about to die (which they will without immediate effective treatment).

Investigation—in early hydrostatic pulmonary oedema, the chest radiograph initially shows distended lymphatics (Kerley septal lines), followed by signs of interstitial oedema such as ‘cuffing’ of airways and arteries. As alveolar oedema becomes established, there is a loss of lucency around the hila in a ‘butterfly’ pattern.

Management—should be aimed at the underlying physiological abnormality where possible, e.g. correction of plasma oncotic pressure or reduction in capillary hydrostatic pressure. General supportive measures involve putting the patient in the ‘trunk up, legs down’ position to help pool blood in the dependent parts and reduce central venous pressure, and giving high-flow oxygen, diuretics, intravenous nitrates, and morphine. If these are ineffective and oxygen administration at normal airway pressure cannot maintain the arterial partial pressure of oxygen and/or hypercapnia develops, then application of a continuous positive airway pressure (CPAP) mask, noninvasive ventilation, or tracheal intubation and intermittent positive pressure ventilation need to be considered.

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