= Solution
\b[The classical sequence in <lobar pneumonia> is <congestion>, red <hepatization>, grey <hepatization>, and resolution.] These are overlapping morphological phases, not a clock that every <pneumonia> follows. An affected <lung> may contain adjacent areas in different phases; <bronchopneumonia> has scattered airway-centred foci rather than uniform involvement of a whole lobe. Modern <antibiotic> treatment often interrupts the textbook sequence.<Pneumonia Pathology in StatPearls>[Histopathology: lobar pneumonia and its four stages]{ref}
During <congestion>, the <lung> is heavy, dark red and boggy but still contains some <air>. Its cut surface gives a blood-stained watery fluid. <Microscopy> shows distended <alveolar capillaries>, <oedema> within <alveoli>, and an early cellular <exudate>, before dense <pulmonary consolidation> has developed. Reduced <alveolar ventilation> begins as fluid replaces the normal air space.
In red <hepatization>, the affected lobe is enlarged, firm, red and substantially airless. Its granular cut surface resembles <liver>, which explains the name; it is not a transformation into <liver> tissue. The <alveoli> are occupied by a mesh of <fibrin> containing abundant <red blood cells> and <neutrophils>, while the <alveolar capillaries> remain congested. Filling of neighbouring air spaces produces continuous <pulmonary consolidation>. Associated <pleurisy> may put a <fibrinous exudate> on the overlying <pleura>.
In grey <hepatization>, <pulmonary consolidation> remains, but the colour becomes grey, grey-brown or yellowish as intact <red blood cells> disappear and the <fibrin> and inflammatory <leukocytes> dominate. <Microscopy> shows degenerating <neutrophils>, debris and persistent intra-alveolar <fibrin>; the conspicuous vascular engorgement of the preceding phase diminishes. Grey colour by itself does not establish a separate pathogen or mean that an <abscess> has formed.<Typical Bacterial Pneumonia in StatPearls>[Histopathology: red and grey hepatization]{ref}
In resolution, the intra-alveolar <exudate> is broken down, ingested by <macrophages>, removed through airways and cleared by absorption. The lobe softens and becomes aerated again. Where the <alveolar septum>[alveolar septa] have survived, the architecture can return nearly to normal; an air-space <exudate> need not become a permanent scar. Failure of clearance may instead lead to organisation and <fibrosis>; destructive infection can produce <abscess> or <empyema>. These are possible outcomes, not obligatory further stages.
A useful examination compares a cut section and a thin <histological section> from each region, following the <alveolar septum>[alveolar septa] to distinguish filling of existing air spaces from destruction of the framework. A dense airless piece may sink in water, but this physical test only shows reduced <air> content: <atelectasis> can also sink. The distribution and the <microscopy> establish why the tissue is airless.
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