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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.^[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.^[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 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 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.