Pathological anatomy and course of lobar pneumonia

1. Gastroepato
2. Pneumology
3. Pathological anatomy and course of lobar pneumonia
4. Pulmonary semeiotics
5. Local complications pneumococcal pneumonia
6. Oxygen therapy
7. Exudative pleuritis

The inflammatory processes of the lung are still the most common observations of the causes of death, which should never be underestimated, especially in patients with myeloproliferative disorders (leukemia, multiple myeloma, etc.), where they often represent the terminal event of systemic processes. debilitating. Although the classification of pneumonia, based on alveolar or interstitial distribution, is still acceptable, an etiological classification is generally preferred.
Bacterial pneumonia is common in the general population, particularly in older people with chronic lung disease or in immunocompromised individuals. Approximately four million cases are recorded annually, of which 20% require hospitalization. Acquired bacterial pneumonitis is associated with a 1% mortality, which increases to 20% in patients admitted to the disease. Several epidemiological studies indicate that streptococcus pneumoniae is the main cause of bacterial pneumonia, followed by hemophilus influenzae and mycoplasma pneumoniae. Other common bacterial agents include chlamydia pneumoniae, staphylococci, streptococcus pyogenes, legionella and other gram-negative bacteria such as pseudomonas, neisseria meningitidis and moraxella catarrhalis.

The same organisms are responsible for both extra-hospital and hospital infections. Streptococcus pneumoniae, legionella, hemophilus influenzae, pseudomonas and Gram negative enterobacteria are however the main causative agents of bacterial pneumonia observed in the Intensive Care Units. Also among the HIV positive subjects, streptococcus pneumoniae is the main cause of bacterial pneumonia followed by hemophilus influenzae, staphylococcus aureus, streptococcus, moraxella catarrhalis and klebsiella pneumoniae.
The diagnostic approach to patients with bacterial pneumonia includes clinical evaluation, followed by radiological and microbiological investigations. The latter are particularly important even if only 5070% are able to confirm the microbiological diagnosis of the infection. Microbiological tests include cytological examination of the sputum or tracheopulmonary aspirate in addition to culture tests.
Sputum examination may not be able to detect the infectious agent, either because about 30% of patients are unable to collect adequate sputum samples, and because many have taken antibiotics. A better result is obtained by examining the tracheobronchial and pulmonary aspirate which allows the causal agent to be detected in 65% of cases. Also with this method, previous antibiotic therapies negatively affect the demonstration of the microorganism. In general, the cytological diagnosis of bacterial pneumonia on sputum or aspirate is suggested when, in a small magnification microscopic field, there is more than 25 neutrophils and less than 10 epithelial cells. The definitive diagnosis must however be placed only with the demonstration of the microorganism in the cytological material. If haematoxylin eosin can be used to demonstrate the presence of nuclear, fungal or protozoal compounds, special stains are of great help in confirming the diagnosis of most bacterial infections. In particular, Gram staining allows to differentiate Gram positive bacteria from Gram negative bacteria; the modified Gram according to BrownHopps is excellent for highlighting Gram negative bacteria and ricketsiae. Colorings with alcohol (Ziehl-Neelsen, Coates-Fite and Fite-Farraco) are useful for mycobacterial tuberculosis and atypical mycobacteria, mycobacterium of leprosy, nocardy and rhodococcus, germs that resist the "alcohol-acid" treatment. The identification of some bacteria may require the use of cultures, immunostaining or immunofluorescence methods, molecular biology techniques with PCR, immunoassay, ELISA and, in difficult cases, electron microscopy.

Anatomic distribution of pneumonia

Based on their anatomic distribution, lobar pneumonia and lobular pneumonia or bronchopneumonia.

Lobar pneumonia

The classic lobar pneumonia, which is observed in prenumococcus infections, can also be produced by other bacteria such as staphylococcus aureus, klebsiella and legionella, although they usually give bronchopneumonic pictures. Streptococcus pneumoniae (pneumococcus) is the most common cause of pneumonia, accounting for about 66% of bacterial forms, although its clinical evolution has been significantly modified by antibiotic therapy. Pneumococcal pneumonia may present as both lobar pneumonia and bronchopneumonia: the first is observed mainly in adults and is supported in most cases by serotypes 1, 2 and 3; the second form prevails in children and the elderly and may be due to any pneumococcal serotype. In the lobar distribution also hypersensitivity phenomena come into play so that lobar pneumonia would arise in sensitized subjects, towards the pneumococcus, from previous pneumococcal infection (rhinitis, otitis, etc.), while in non-sensitized subjects pneumococcal pneumonia would take the form of bronchopneumonia. The allergic pathogenesis of lobar pneumonia would explain the sudden onset of the disease, the rapid extension of the inflammatory process to the affected lobe, resolution by crisis, the cyclical character, as well as the frequency with which the pneumonia tends to repeat itself in the same subject.

At the onset of pneumococcal pneumonia, usually sporadic and only occasionally epidemic in some municipalities (schools, barracks, etc.), other conditions such as upper respiratory tract infections, alcoholism, inhalation of irritating gases, diabetes, immunodeficiency states and any condition that compromises the cough reflex (eg coma). Pneumococcal infection is essentially an endogenous infection due to alteration of the defense mechanisms of the respiratory tract, designed to prevent the spread of infectious agents from the nasopharynx to the lung where they cause acute inflammation.
The classic manifestation of pneumococcal pneumonia is lobar pneumonia, which is clinically characterized by a sudden onset with shivering followed by abrupt elevation of the temperature, thoracic puncture pain, cough, blood sputum, tachypnea with hypophonesis and rattling rattles. Neutrophilic leukocytosis is often associated and in many cases pneumococcus can be isolated in blood cultures. Cyanosis appears in an advanced stage of the disease.
In the anatomopathological evolution of the process, before the introduction of antibiotic therapy, there were classically four evolutionary stages that included:
- the hemorrhagic congestion,
- red hepatization,
- gray hepatization
- the resolution.

The same patient but the chest X-ray documenting pleural effusion, in the left basal area, which is associated with extensive parenchymal tapering in the middle and lower ipsilateral fields

The antibiotic therapy has broadly modified the natural course of the process reducing both the incidence and mortality, for which the classically described anatomopathological aspects are rarely observed. As a rule, lobar pneumonia affects only one lung lobe but may involve several lobes simultaneously or in succession; the right lung and the lower lobes are preferred.
In the stage of hemorrhagic engorgement, which generally lasts less than 24 hours and which is rarely observable at the anatomic table, the affected lobe is somewhat increased in volume and consistency and appears dark red in color; from the cutting surface comes a large amount of serum, poorly aerated liquid, for this reason fragments of fabric placed in water tend to sink slowly. Histologically, they dominate the intense dilation of the alveolar capillaries, which are congested, and the presence in the alveolar cavities of a serum exudate (with few alveolar macrophages and rare granulocytes), often rich in pneumococci. The vascular engorgement is truly impressive and is not reflected in any other morbid condition, including pulmonary stasis, where the endoalveolar serum exudation is lacking; the vessels appear to be artificially injected and protrude into the alveolar lumen.
The next stage of red hepatization, which begins mostly on the second day and lasts for 23 days, is microscopically characterized by an increase in volume and consistency of the entire lobe completely free of air, so it is assuming a compactness similar to that of the liver (hence the term "hepatization"); the cut surface, of dark red color, is dry and granular (the granularity is due to the protrusion of the sapphires, of fibrin from the alveoli and from the alveolar ducts in elastic retraction due to the cut) and the fragments of the lung immersed in the water are quickly to the bottom; the visceral pleura of the affected lobe, which appears reddened and already opacified in the 1st stage (whence the puncture pain), is now covered by easily removable fibrin veins, expression of fibrinous pleurisy that accompanies the lobar pneumonia.
The alveoli appear full of red blood cells and partly also of neutrophil granulocytes, chemiotactically recalled and included in the mesh of fibrin network. The capillaries are still engorged, but hyperemia tends to fade. In this stage the phenomena of phagocytosis of the pneumococci by the granulocytes begin, without however that the germs disappear. The bronchi are intact or have usually modest signs of catarrhal or serofibrinose inflammation.
In the third stage or stage of gray hepatization, whose acme usually coincides with the fifth day of disease, fibrinous exudation and migration of neutrophil granulocytes touch the maximum values, while the diaphragms of the red blood cells come to an end. The gradual transfer of red and gray hepatization depends on: 1) the pressure of the endoalveolar exudate, which compresses the septal capillaries ischemizing the inflamed tissue, 2) from the progressive increase of fibrinoleucocyte exudation, 3) from the hemolysis of red blood cells contained in the endoalveolar exudate.
At this stage, the increase in volume, weight and firmness of the affected lobe reaches the maximum extent; fibrin pleuritis is also more evident. The cutting surface is very grainy and reddish or quite greyish. In more advanced phases it is possible, due to phenomena of fatty degeneration of the leukocytes, that the hepatized lobe has a yellowish tinge or a decidedly yellow chromatic tonality, so that it is called yellow hepatization; however, this is not an obligatory stage of pneumonia. On histological examination, the alveoli appear to be distended by the fibrinosoleucociliary exudate and the thin and blood-rich interalveolar septa, the abundant fibrin no longer forms a small reticule, but is collected in a coarse plot and it is also possible to see fibrin filaments pass through the alveolar walls passing through the Kohn porocanalicoli; the red blood cells have disappeared or visible as shadows, while pressure, an abundant exudate roseogrigiastro or even gray-greenish, commited to fine air bubbles, a finding that can recall the pus, but it is not pus; fragments of fabric, immersed in water, tend to float or slowly go to the bottom.
The histological finding varies according to the phase reached by the resolution process. At the beginning there is a splitting of the fibrinous network and the granulocytes, still recognizable, appear maladaptive and prey to regressive processes; with the continuation of the lysis, the fibrin turns into granular debris that can be incorporated by the macrophages, while the granulocytes undergo disintegration, remaining only chromatinic debris. Where the process is even more advanced, the alveoli tend to resume normal appearance as there is no alveolar destruction.
The elimination of fluidized exudate occurs partly by air, by expectoration with coughing, and partly, which is considered prevalent, by lymphatic and blood.
The overall duration of the entire morbid picture, from the beginning to the appearance of the critical resolution, in cases with natural evolution and not modified by chemioantibiotical therapy, is about 79 days, but it may be prolonged by the introduction of new outbreaks of hepatisation in pulmonary areas near or far from the one initially affected (migrating pneumonia).
It should be emphasized that the anatomical resolution of the pneumonitis process does not always correspond to the clinical resolution of the disease which in the typical cases occurs dramatically due to seizures in the 5th or 7th or 9th day (rarely later or due to lysis) and which occurs with sudden fall in temperature accompanied by profuse sweating, disappearance of physical signs of hepatization (dullness, bronchial breath) and the reappearance of wet rales (crepitatio redux). In fact, we must remember that between the anatomical and clinical resolution of the disease there is no close interdependence, although both phenomena are related to the immunological changes that the infectious process induces in the organism during its evolution; although often coinciding, the crisis may not be synchronous with the local resolution, because the dissolution and re-absorption of the exudate also depend largely on local factors. These rare discordances have become very frequent in the age of antibiotics, which essentially act as an obstacle to the development of pneumococci, without favoring the anatomical resolution of the process itself. It should also be noted that the resolution of the process is slower in patients with bacteraemia, the elderly, smokers and in subjects with other chronic pulmonary or cardiac diseases. In the latter, as well as in subjects with malignant neoplasms, cirrhosis of the liver, extrapulmonary diffusion of pneumococcal infection and in patients with drug resistance, mortality is increased. The use of the pneumococcal vaccine in patients at risk (children under 2 years of age, adults aged over 65 with chronic diseases and immunosuppressed subjects) covers almost 90% of the serotypes responsible for pneumococcal infection in adults and 100 % of those responsible for pneumonia in children. Potential complications of pneumococcal pneumonia are rare (15%) and may be local as carnation, lung abscess and empyema, or as systemic as metastatic infections that can cause meningitis, endocarditis, arthritis or cellulitis.

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