Pulmonary Oedema

Introduction

This is a disease characterised by excessive fluid in the lung. Normally, mechanisms are in place to protect the lung from the entry of circulatory fluid into alveolar spaces (See functional anatomy). This occurs when exudation of fluid from vessels into interstitium or alveoli exceeds the rate of alveolar or lymph removal and is generally a sequel to or part of congestion or inflammatory process. The process generally begins as interstitial oedema characterised by expansion of perivascular and peribronchial and peribronchiolar fascia and distension of interstitial lymphatics. Only when this interstitial compartment is overwhelmed does fluid flood the airspaces causing alveolar oedema.

The lungs appear heavy and wet and do not properly collapse. There is presence of subpleural and interstitial tissue distended with fluid and foamy fluid oozing from the cut surface and airways will be present.

Pinkish fluid in alveoli and airways in association with air bubbles, and also in dilated lymphatics of the interstitium

Colour of the fluid enhanced in cases where the endothelium is damaged - more protein present

In slowly developing cases, macrophages contain haemosiderin

The major causes of pulmonary oedema are:

Increased capillary or type I epithelial permeability caused by

Systemic toxins

Shock

Inhaled caustic gases

Increased capillary hydrostatic pressure (cardiogenic oedema - left-sided or biventricular heart failure, sympathetic stimulation in acute brain damage)

Decreased plasma oncotic pressure (hypoalbuminaemia)

Overloading in excessive fluid therapy

As part of inflammatory process

• In the normal state, pulmonary alveoli are kept dry by three mechanisms:
  1. Normal "push-pull" mechanism at capillary level.
  2. Efficient lymphatic drainage by rhythmic pumping action near airways.
  3. Integrity of the alveolar epithelial basement membrane is relatively impermeable.
     • Unlike the capillary basement membrane, which is relatively permeable.

Pathogenesis

1. The pumping efficiency of the lymphatics is exceeded.
2. Fluid accumulates in connective tissue adjacent to airways.
3. The alveolar walls fill with fluid.
4. The alveoli abruptly and severely fill with fluid.
   • Associated with the disintegration of alveolar epithelial junctional complexes.

Haemodynamic type

• Fluid leaks into alveoli via junctional complexes BUT the alveolar basement membrane remains intact.
  • I.e. is due to elevated pulmonary venous pressure.
• Potentially reversible.
• Causes:
  1. Cardiogenic
     • Usually left ventricular failure.
     • Also occurs with cardiac overload due to valvular disease.
  2. Mechanical
     • Large primary pulmonary tumours.
     • Severe metastatic disease.
     • Granulomatous infections may raise pulmonary venous pressure.
  3. Neurogenic
     • Seizures or CNS disorder.
     • Rare in domestic species.

Permeability type

• Fluid fills the alveoli following damage to cells or junctional complexes, or permanent ionic alteration of the alveolar basement membrane.
• Irreversible.
• Causes:
  1. Toxins
     • Bacterial
       • Pseudomonas
       • Pasteurella
       • Staphylococcus
     • Chemical
       • Paraquat.
  2. Aspiration/inhalation
     • Gastric contents (low pH)
     • Smoke.
     • Excess ozone.
     • Oxygen.

• There may be a combination of haemodynamic and permeability types in electrocution syndromes and "shock" lung.
  • E.g. in Adult Respiratory Distress Syndrome (ARDS).