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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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