Alveolar disease

• What are the types of alveolar disease?

  • Aspiration pneumonia
  • Pulmonary oedema (cardio vs non-cardiogenic)
  • Pulmonary haemorrhage
  • Eosinophillic lung disease
  • Pulmonary parasites
  • Pulmonary neoplasia - primary/ metastatic
  • Infectious pneumonias.
• Clinical signs of pulmonary parenchymal disease

  Usually increased inspiratory and expiratory effort.

  Cough may or may not be present.

  Can less frequently hemoptysis, collapse/syncope or cyanosis.

  Occasionally minimal signs of respiratory disease are noted even with severe pathology - particularly in cats.
• What is aspiration pneumonia?

  Inhalation of material into the lower airway. Stomach contents with variable amounts of particulate matter. Care with nursing recumbent patients. Primary infection due to aspiration is less common.
• Signs for aspiration pneumonia

  Cough - harsh/ reduced lung sounds, tachypnoea, pyrexia.

  Check oxygenation - serial elevation.

  On radiographs - alveolar infiltrate (patchy/focal). Most common affected lobes are right middle, right cranial and left cranial.

  
• Treatment of aspiration pneumonia

  Supportive - oxygen therapy, antibiotics (care with oxidative damage to already fragile lung).

  Treat any underlying cause.

  Consider anti-acid medication if frequent occurrence.

  may increase gastric bacterial load.

  Metoclopramide to improve motility and increase LOS tone.

  Alveolar pattern - border obliteration, air bronchograms.
• Antibiotics for respiratory tract disease

  Antibiotic selection should ideally be based on C&S. Require high concentration in the lungs. Need to penetrate, dissolve in blood-bronchus barrier (Lipophilic antibiotics penetrate this best). Ensure adequate treatment period at least 4-6 weeks for severe/ chronic infections. Primary infection is uncommon in dogs.
• Type of antibiotics for respiratory tract disease

  Fluoroquinolones are connected significantly in canine alveolar macrophages good penetration into airway.

  Macrolides are reasonably well concentrated into respiratory tract.

  Lincosamides - accumulate well in phagocytes.

  Penicillins have relatively poor distribution into bronchial tissue.

  Cephalosporins - variable penetration depending on generation although better than penicillins.

  Tetracyclines - reasonable concentration in secretions relative to plasma.
• Pulmonary oedema

  Consequence of various conditions - increased hydrostatic pressure, reduced oncotic pressure, increased vascular permeability, impaired lymphatic drainage.

  This leads to fluid accumulation in the interstitium and subsequently in the alveoli at a rate that exceeds removal.
• Cardiogenic pulmonary oedema

  low protein due to increased hydrostatic pressure without increased vascular permeability
• Non-Cardiogenic pulmonary oedema

  The result of lung damage which increases vascular permeability so protein leaks out.

  Increased vascular permeability, higher protein fluid in alveoli, removal of the fluid requires active transport of sodium and chloride from the luminal surface across epithelial cell to the basal surface.

  This is an active process - if the epithelium is damaged this cannot occur.

  So the damage to the epithelium leads to fluid accumulation and reduced the ability to remove the fluid which makes non-Cardiogenic oedema more refractory to therapy than Cardiogenic oedema.
• Eosinophillic lung disease - EBN

  More common in dogs, with reactive eosinophillic airway disease occurring in cats.

  Radiographs show diffuse bronchointerstitial pattern although can see alveolar patterns (can be dense infiltrates).

  Circulation eosinophilia in ~50% dogs - some will have hyper eosinophillic syndrome.

  BAL for diagnosis - caution to look for parasites, neoplasia and fungal disease.
• Treating EBN

  Prednisolone 1-2mg/kg daily.

  Outcome - often very good unless other organs involved in which case prognosis guarded.
• Angiostrongylus vasorum

  Nematode, this is a vascular worm. Adults live in the pulmonary arteries. indirect lifecycle, the dog is definitve host/slug or snail is intermediate host.
• Life cycle of A. vasorum

  • L1 penetrates capilliries and alveolar wall.
  • L1 coughed up and swallowed.
  • L1 in faeces.
  • L1-L3 develop in snug/snail.
  • Dog eats slug/ snail or secretion/ faeces.
  • Stomach/ small intestine.
  • L5 Mesenteric lymph nodes
  • Migration via lymphatics to hepatic portal vein/ liver.
  • Vena cava
  • Right ventricle
  • Adult in pulmonary artery
  • Eggs in pulmonary capillaries - clinical signs.
• Clinical signs of A. vasorum infestation

  Often complex presenting signs, not limited to the respiratory tract - early stages of infection are often asymptomatic, recent established infections signs may also be minimal.

  Cardiorespiratoy - the degree of signs is associated with the worm burden.

  Coagulopathies - anaemia, subcut haemotmas, internal haemorrhages, prolonged bleeding from wounds or after surgery, thrombocytopenia.
• Diagnosis of A. vasorum

  Can be difficult to diagnose. Radiograph may show alveolar infiltrates, routine biochemistry - generally unremarkable (occasionally see Hypercalcaemia).

  CBC - eosinophilia, increased APTT/OSPT, thrombocytopenia.

  Eosinophilic inflammation on BAL fluid.