Chapter: Medicine Study Notes : Respiratory

Acute Interstitial Lung Disease

Adult Respiratory Distress Syndrome (ARDS)

Restrictive/Interstitial Pulmonary Disease

· = Reduced expansion of the lung parenchyma

· British and Americans give them different names

· Over 150 different disease processes primarily affecting alveoli epithelium, interstitium and capillary endothelium, not airways

· Leads to ¯expansion of lung parenchyma, ¯total lung capacity, ¯lung compliance

· Other causes:

o Secondary to drugs (eg amiodarone)

o Secondary to radiotherapy

o In some connective tissue diseases (eg Ankylosing Spondylitis)

Acute Interstitial Lung Disease

Adult Respiratory Distress Syndrome (ARDS)

· = Diffuse Alveolar Damage (DAD)

· = Shock Lung

· Clinical: rapid onset of life-threatening respiratory insufficiency, cyanosis and hypoxaemia refractory to O₂ therapy

· Diagnostic criteria: acute onset, fluid on CXR, capillary wedge pressure < 19 (Þ not LH failure), hypoxia

· Aetiology – types of injury:

o Aspiration: gastric contents or drowning

o Inhalation of fumes or toxic aerosols, smoke, chlorine, oxygen toxicity

o Circulating toxins: bacterial endotoxins

o Other: DIC, high altitude, trauma, radiation therapy, chemotherapy

· Pathogenesis:

o Results from leakage from capillaries to alveoli spaces: non-cardiogenic pulmonary oedema

o Leads to a non-compliant lung: smaller tidal volume, poor gas exchange, risk of lung rupture when ventilating

o Prototypical injury is oxygen toxicity: hyperoxia damage alveolar macrophages (AM) ® release O₂ radicals ® injure lung tissue; AM release cytokines ® attract neutrophils, stimulate intravascular adherence, and release further O₂ radicals. Vicious circle of damage, especially to septum

o Other possible initiating mechanisms (alone or in combination): activation of complement cascade, neutrophil aggregation, activation of coagulation ® fibrin deposition, etc

· Macroscopic appearance: Affects WHOLE lung (if only one lobe affected ?pneumonia). Heavy lungs due to fluid accumulation (interstitial and later alveolar)

· Microscopic appearance:

o Early change: interstitial oedema, few cell infiltrates

o Acute exudative stage: microvascular injury ® breakdown of basement membrane ® leakage of plasma proteins into alveoli. Sloughing of injured type 1 pneumocytes. Cell debris + exudate form hyaline membrane. Inflammatory cells in interstitium. No neutrophils in alveoli (key differential from pneumonia)

o Proliferative stage: Type II pneumocytes proliferate to cover alveolar surface. Fibroblasts lay down collagen in interstitium and alveolar spaces ® interstitial and intra-alveolar fibrosis

· Prognosis: 50% mortality. Surviving patients may have mild to extensive diffuse interstitial pulmonary fibrosis

Acute Interstitial Pneumonia (AIP)

· = Hamman-Rich Disease

· Rapidly progressive interstitial pneumonitis that resembles the organising stage of DAD (?may be a variant)

· Affects young adults, presenting with flu-like syndrome and bilateral infiltrates. Most die of respiratory failure within two months

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Medicine Study Notes : Respiratory : Acute Interstitial Lung Disease |