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.
It represents an abnormal evolution of the infectious process in focal scar or
in diffuse parenchymal fibrosis; is observed more frequently after the
introduction of antibiotic therapy and occurs in those cases, infrequent, in
which contrary to the rule is missing, in whole or in part of the affected lobe,
the dissolution and reabsorption of the endoalveolar exudate, fibrinous in
particular, for which this is gradually organized by a newly formed connective
tissue, initially young, rich in fibroblast, and therefore increasingly compact
and poor in cells, until it has a scar-like appearance. It is characteristic
that in celled areas the alveolar structure remains recognizable for a long time.
The lack of lysis of fibrin, an essential condition for the organization of the
exudate, has causes that to date can not be specified, given the uncertainties
still existing on the factors determining the critical resolution of the
pneumonia process. Poor proteolytic enzymatic activity of polymorphonuclear
leukocytes, defect of opsonins or antibodies favoring phagocytosis and
destruction of pneumococci, inertia of alveolar macrophages, previous
obstruction of lymphatic drainage pathways, circulatory stasis, etc. they are,
in theory, local factors that could come into play in individual cases, in
isolation or synergistically. Although there is no obvious reason, two factors
favor the development of fibrosis:
1. bronchial obstruction associated with necrosis of the alveolar tissue;
2. thrombotic or embolic obstruction of the arterial branches affecting the
affected area. Also at the protraction of pneumococcal infection was given
importance as a pathogenetic moment of the process of carnation.
Macroscopicammte, the "carnated" areas are compact, consistent, airless, of
rose-redish color, with a shining surface with a fleshy appearance; frequent
pleural adhesions. The histological finding varies according to the evolutionary
stage of the organization process. At first the fibrin becomes more compact and
intensely eosinophilous and more or less numerous alveolar macrophages appear,
while the leukocytes undergo fatty degeneration; subsequently, starting from the
periphery of the fibrinous hoof, young fibroblasts and fine reticular fibrils
invade and progressively replace the fibrin reticulum, filling the alveolar
lumen and extending through the porocanalicoli to the neighboring alveoli; in an
even later phase, the newly formed connective tissue is depleted of cellular
elements and, due to the appearance of collagen fibers, is transformed into an
adult connective of cicatricial appearance. The honeycomb panels are always well
recognizable, but they can
Although in the advanced stages of pneumonia the exudate assumes purisimile
character (due to the abundance of the leukocyte share and the fatty
degeneration of the leucocytes themselves), we can not speak of suppurative
evolution as the interalveolar septa and the interstitial connective preserve
their integrity . When, on the other hand, as an outcome of an infection with
very virulent germs, especially in cases of pneumococci infection of serotype 3,
or of poor organic resistance, or a secondary plant of pyogenic germs in the
pneumonia outbreaks, the alveolar walls, sometimes already in the stadium of
gray hepatization, they undergo necrosis and purulent fusion: they constitute
real purulent collections (parapneumonitic abscesses). Small abscesses are
macroscopically visible as yellowish patches with a creamy content; the
voluminous abscesses, which often derive from the confluence of small
suppurative outbreaks, appear as anfractuose cavities filled with yellowish pus,
within a still-hepatized lobe. Frequent is their opening in a bronchus or, if in
the subthreshold, in the pleural cavity (with consequent empyema). The abscess
formations can persist or appear even after the resolution of pneumonia (metapneumonic
abscesses). When anaerobic germs are implanted in the abscess foci, so does the
pulmonary gangrene. The gangrenous areas have greenish color and give off a
fetid odor.
Since in the course of lobar pneumonia there is constant, from the initial
stages (pain point!), A reactive fibrinous pleurisy mostly localized to the
affected lobe or lobes, it is not correct to consider pleurisy as a complication
of pneumonia. A true pleural complication can only be used when the pleural
exudate has a purulent character (pleural empyema). The empyema may occur during
the stages of hepatization (parapneumonic empyema) or at a successful resolution
(metapneumonic empyema). Pus is usually rich in pneumococci that reach the
pleura by the lymphatic route, but there are also mixed empyema, which mostly
follow a pulmonary abscess and are prognostically much more severe. Purulent
inflammation can be propagated, by contiguity and by lymphatic route, to the
connective lupus of the mediastinum (purulent mediastinitis) and to the
pericardium (purulent pericarditis). The pus can be emptied in the bronchi or
outside (empiema necessitatis). Extended cases of pleural rupture remain in the
healed cases, possibly with calcification.
In many cases pneumococcal pneumonia (20-35%) occurs bacteriemia or septicemia
which can sometimes lead to the appearance of severe complications that include:
a) valvular endocarditis (aortic and mitral) with possible septic embolisms and
formation of brain abscess in particular;
b) purulent meningitis which mainly affects the vault; the association of lobar
pneumonia, endocarditis and meningitis constitutes the triad of Marchiafava;
c) septic arthritis, generally solitary and localized to large joints;
d) peritonitis and purulent pericarditis may occasionally present themselves as
phenomena of a local extension of the infectious process or by lymphatic
diffusion.
More frequent than lobar pneumonia, from which it differs mainly due to the
outbreak distribution of pulmonary inflammation, it often affects both the lungs
and the lower lobes in particular; hence the more comprehensive term of outbreak
pneumonia. It is also called lobular pneumonia, but bear in mind that the
affected regions may be smaller or larger than the lobules. The term
bronchopneumonia is linked both to the participation in the practically constant
inflammatory process of the bronchial system (which contrasts sharply with what
occurs in lobar pneumonia, where the bronchi are normally free), yes to the fact
that often the bronchial inflammation precedes chronologically and
pathogenetically alveolar inflammation. However, there is no shortage of
pneumonia in outbreaks of undoubted blood origin (eg during sepsis).
Bronchopneumonia is a disease especially of infancy and old age. It is believed
that this depends largely on the immunological conditions of the subject, being
recognized that the state of anergy favors the onset of bronchopneumonia,
whereas lobar pneumonia corresponds to an allergic hyperergic situation.
In infancy, bronchopneumonia usually arises as a complication in pertussis,
measles, scarlet fever, diphtheria, varicella, etc., and in children with
nutritional disorders. Even in adults and older bronchial pneumonia usually has
a secondary character, observing often, as a terminal complication during severe
tossiinfettive diseases, debilitating chronic diseases (heart disease,
decompensated, chronic kidney disease, liver cirrhosis, diabetes, cancer, blood
disorders, etc.) and following surgical interventions, protracted narcosis,
trauma, etc.
In the genesis of these secondary bronchopneumonia are important predisposing
factors:
a) circulatory disorders (chronic pulmonary stasis); it is above all the long
lasting hypostasis which, through the edema and the congestion of the lungs,
creates favorable conditions for the development of bronchopneumone outbreaks in
the sloping areas of the lung;
b) defective pulmonary ventilation, in particular responsible for the
distelectatic brocopneumonitis of infants, of bronchopneumonia which develop in
atelectatic territories (atelectatic bronchopneumonia) or which arise after
surgical interventions in the upper abdomen or following severe chest injuries;
c) the suction of infectious material (mucus, blood, food substances, foreign
bodies, etc.) favored by conditions that obstruct the swallowing and the
reflection of the cough (comatose states, paralysis buibare, paralysis of the
hanging veil, ulcerative lesions of the first ways aerial and digestive):
bronchial pneumonia ab ingestis or aspiration, often of an ascascular and
gangrenose type.
This category also includes certain forms of nonspecific bronchopneumonia from
postemofthial aspiration that occur following copious hemoptysis (from pulmonary
caviar tuberculosis, lung abscess, bronchiectasis, pulmonary neoplasias, etc.)
or from penetration into the bronchi of blood from the upper airways, from the
stomach etc. In the case of cavitary tuberculosis due to the presence of
mycobacteria in the aspirated blood, the formation of a caseous bronchopneumonia
may occur.
In addition to the secondary bronchopneumonias now remembered, extremely
frequent and complicating the most varied morbid conditions, there are also
primitive bronchopneumonitis that affect healthy subjects and in which,
alongside the microbial agents, the perogigerations, the inhalation of
irritating, smoke and gases, toxic vapors etc.
The macroscopic finding is very variable from case to case, due to the number,
extent and intrinsic characteristics of the parenchymal thickening outbreaks.
Usually the affection is bilateral, although the alterations may be more serious
on the one hand, and affect the lower lobes more. The areas of pulmonary
thickening often better recognizable at palpation, due to the non-homogeneous
increase in consistency and to the reduction of crackling in the affected areas,
rather than to direct vision appear on the sectional surface as outbreaks of
different number and size but as a rule of dimensions not superior to those of a
lobule, slightly prominent, with faded outlines and have a variable color from
dark red to rosy-greyish or clearly gray, and a consistency variously increased
compared to the healthy parenchyma; these areas, which sometimes have a granular
appearance, are free of air and sink into the water.
In many cases the bronchopneumone outbreaks are very extensive and close
together and can merge (bronchial pneumonia to confluent outbreaks), to occupy a
large part or even an entire lobe (pseudolobare bronchopneumonia). When this
occurs, the affected areas rarely have an uniform evolution and color characteristic of lobar pneumonia in which all the areas
of the lobe involved in the process are affected simultaneously. The involvement
of the bronchi is practically constant and it is often possible to squeeze out
mucopurulent exudate droplets even from the finest bronchiolar branches. When
the bronchopneumone focuses are superficial, the pleura often appears to be
covered by fibrinous stratifications.
Histologically, the scarcity or absence of fibrin and the extreme morphological
variability of the endoalveolar exudate are characteristic of bronchopneumonia.
In fact, the serous or hemorrhagic component or the abundance of alveolar
macrophages or neutrophil granulocytes dominate from time to time; these various
aspects often coincide in the same outbreak or in nearby outbreaks, so that a
subdivision into stages of the alveolar inflammation is not possible (as a rule,
the typical cyclic course of lobar pneumonia is clinically missing). In
non-confluent areas, the alveoli interposed between the various outbreaks are
the site of congestive and edematous phenomena, while in confluent forms it is
possible to recognize that the process derives from the fusion of single
outbreaks, also through the variability of the endoalveolar cytological finding
in contiguous areas.
At the center of the bronchopneumone outbreaks it is almost always possible to
find a small bronchus with the lumen occupied by mucopurulent exudate and with
inflammatory infiltration of the walls, but not always the alveoli, site of the
inflammatory process, topographically correspond to the affected bronchus.
The histological characters of the endoalveolar exudate in bronchopneumonia
depend, in addition to the particular action of the germs in question, on the
age at which the individual is affected, in relation to the modification of the
immunobiological situation. In surviving infants a few hours or days (in which
an infection contracted in the intrauterine life or during labor is to be
assumed), bronchopneumonia, due to the poor reactivity of the tissues, is
characterized by a serogranulocyte exudate.
Pneumology