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Complications of pneumonia: 1. Delayed resolution. 2. Abscess formation . 3. Empyema 4. Organization of exudates with fibrosis. 5. Bacteremia & septicemia with infection to other organs e.g. endocarditis, pericarditis, meningitis, arthritis etc. |
A painful pleuritis is common because the pneumonia often extends to the pleura.
There is usually a small pleural effusion, which resolves.
However, this may occasionally be large and purulent (pyothorax) and may heal with extensive fibrosis.
Rarely, the purulent exudates persists and leads to a loculated collection of pus with fibrous walls (empyema).
Bacteremia is usually present in the early stage and may result in endocarditis or meningitis.
(Infective Endocarditis ; Meningococcal Infection)
Rarely, the alveolar lesion proceeds to fibrosis, in which case the intra-alveolar exudates becomes organized as fibroblasts leads to a shrunken and firm lobe, a rare complication known as “carnification”.
Another uncommon outcome is a lung abscess.
Little is known about the precise pathogenesis of pneumococcal pneumonia.
The frequency of a previous respiratory tract infection suggests that impairment of airway clearance mechanisms may be important.
It has been suggested that the organisms can multiply rapidly in the increased airway mucus and may then be aspired into the periphery.
The remarkably severe acute inflammation with spreading edema has led to speculation that immunologic mechanisms may be involved
Cause of death: Toxemia with peripheral circulatory failure.
Treatment : Penicillin (penicillin G/amoxicillin) remains the drug of choice for strains that are fully sensitive or have a moderately decreased susceptibility to penicillin, whereas cefotaxime and ceftriaxone are the first-line alternatives in cases with higher levels of resistance.
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Causative organism
of Lobar Pneumonia: (1)Pneumococcus - type I, II, and III are responsible for 90% cases. Type III pneumo- cocci are most virulent & mainly seen in patients over 50 years of age. (2) Occasionally, Friedlander’s pneumobacillus. |
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Pathogenesis: Sudden onset & pathological changes suggest the role of hypersensitivity in the pathogenesis. Previous infection sensitizes the lungs, so that subsequent infection may result in pneumonia. Pneumococci reach alveoli via bronchial tree. They pass in the inflammatory fluid from one alveolus to another through the alveolar pores of Cohn. Thus infection spreads throughout the entire lobe. Edema producing substances of capsular polysaccharide cause marked inflammatory edema with acute inflammatory exudates filling up alveoli. The lung is converted into a solid & airless organ.The process is known consolidation or hepatization (liver-like in consistency). |
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Pathology: 1.Congestion: Gross: (i) Lungs are dark-red color & pits on pressure (due to edema). (ii) Cut surface: bloodstained frothy fluid comes out. Microscopic features: (i) Alveolar capillaries are dilated. (ii) Alveoli contain edema fluid & pneumococci. (iii) Air is still present in the alveoli. 2. Red hepatization: Gross: (i) Affected part of the lung is consolidated, reddish-brown & sinks in water. It is friable. (ii) Outer surface is covered with fibrinious exudates. (iii). Cut surface is rough, dry & granular. Microscopic feature: i) Alveoli are airless & filled up with inflammatory exudates consisting of RBCs, neutrophils & fibrin strands. ii) Alveolar wall is thick (due to edema) with congested blood vessels (In low power -mosaic appearance) 3. Grey hepatization: Gross: (i) Consolidated part is gray colour & more friable. (ii) In outer surface pleural exudates is thicker. (iii) Cut surface is moist & brownish-gray colour (bronchial lymphnodes may be enlarged). Microscopic features: (i) Alveolar exudates have lost their freshness (due to action of proteolytic enzymes). RBCs are ghosts, nuclei of polymorphs are broken & indistinct and fibrin threads contract to form a clear zone adjacent to alveolar wall. (ii) Alveolar wall is thin (due to lack of edema) and congested blood vessels disappear. 4.Resolution: Gross: Lung is soft & translucent (jelly like). Microscopic features: (i) Macrophages invade exudates. (ii) Alveolar exudates is liquefied by proteolytic enzyme & removed. Thus the consolidated lung is restored to normal. |
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