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Pulmonary oedema

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Noncardiogenic pulmonary oedema

Aetiology

Due to imbalance of Starling’s forces

  • hypoalbuminaemia. Balance in favour of inward movement of fluid is usually so great that even with severe hypoalbuminaemia a rise in pulmonary capillary pressure or a fall in interstitial pressure is necessary to produce pulmonary oedema
  • negative interstitial pressure:
    - re-expansion pulmonary oedema
    - acute airway obstruction

Due to decreased lymphatic drainage

  • lymphangitis carcinomatosis
  • lung transplant
  • fibrosing lymphangitis (eg silicosis)

Due to increased pulmonary capillary permeability

Due to incompletely understood mechanisms

Re-expansion pulmonary oedema

Risk factors

- chronic collapse (>3 days)
- large volume of air/pleural fluid evacuated
- rapid re-expansion
- ? markedly negative intrathoracic suction

Mechanism

- negative interstitial pressure
± increased alveolar capillary permeability. ? reperfusion injury, ? deprivation of oxygen and nutrients whilst collapsed, ? surfactant deficiency

Tocolytic induced pulmonary oedema

Occurs in up to 4.4% of pregnant women who receive tocolytics (beta agonists eg terbutaline, ritodrine).

Pathophysiology

- controversial
- probably hydrostatic rather than due to increased capillary permeability

Possible risk factors

- multiple gestations
- pre-eclampsia
- sepsis

Clinical features

- pulmonary oedema can occur during administration or after discontinuation
- frequently associated with volume overload

Management

- oxygen, diuretics and discontinuation of tocolytic

Neurogenic pulmonary oedema

  • well described following convulsions and following catastrophic traumatic brain injury
  • syndrome following less severe brain injury less clearly defined
  • thought to be related to massive sympathetic discharge with peripheral vasoconstriction and shift of blood into central circulation. Combined with fall in LV compliance causes left atrial hypertension and hence pulmonary oedema.

Narcotic induced

  • previously thought to be due to impurities in illicitly obtained narcotics but has been reported following overdose of legitimately obtained morphine, methadone and dextropropoxyphene

High altitude

  • probably combination of hypoxia induced pulmonary arteriolar constriction and exercise induced increase in cardiac output and pulmonary artery hypertension. Results in pre-arteriolar high pressure pulmonary oedema

 


© Charles Gomersall December 1999

 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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