S. Pneumoniae Produces Local Edema That Aids in The Proliferation of Organisms and Their
S. Pneumoniae Produces Local Edema That Aids in The Proliferation of Organisms and Their
PATHOGENESIS.
The lower respiratory tract is normally kept sterile by physiologic defense mechanisms,
including the mucocil iary clearance, the properties of normal secretions such as secretory
immunoglobulin A (IgA), and clearing of the airway by coughing. Immunologic defense
mechanisms of the lung that limit invasion by pathogenic organisms include macrophages
that are present in alveoli and bronchioles, secretory IgA, and other immunoglobulins.
Viral pneumonia usually results from spread of infection along the airways, accompanied by
direct injury of the respiratory epithelium, resulting in airway obstruction from swelling,
abnormal secretions, and cellular debris. The small caliber of airways in young infants makes
them particularly susceptible to severe infection. Atelectasis, interstitial edema, and
ventilation-perfusion mismatch causing significant hypoxemia often accompany airway
obstruction. Viral infection of the respiratory tract can also predispose to secondary bacterial
infection by disturbing normal host defense mechanisms, altering secretions, and modifying
the bacterial flora.
When bacterial infection is established in the lung parenchyma, the pathologic process varies
according to the invading organism. M. pneumoniae attaches to the respiratory epithelium,
inhibits ciliary action, and leads to cellular destruction and an inflammatory response in the
submucosa. As the infection progresses, sloughed cellular debris, inflammatory cells, and
mucus cause airway obstruction, with spread of infection occurring along the bronchial tree,
as it does in viral pneumonia.
S. pneumoniae produces local edema that aids in the proliferation of organisms and their
spread into adjacent portions of lung, often resulting in the characteristic focal lobar
involvement.
Group A streptococcus infection of the lower respiratory tract results in more diffuse
infection with interstitial pneumonia. The pathology includes necrosis of tracheobronchial
mucosa; formation of large amounts of exudate, edema, and local hemorrhage, with extension
into the interalveolar septa; and involvement of lymphatic vessels and the increased
likelihood of pleural involvement.
S. aureus pneumonia manifests in confluent bronchopneumonia, which is often unilateral and
characterized by the presence of extensive areas of hemorrhagic necrosis and irregular areas
of cavitation of the lung parenchyma, resulting in pneumatoceles, empyema, or, at times,
bronchopulmonary fistulas.
Recurrent pneumonia is defined as 2 or more episodes in a single yr or 3 or more episodes
ever, with radiographic clearing between occurrences.
CLINICAL MANIFESTATIONS.
Viral and bacterial pneumonias are often preceded by several days of symptoms of an upper
respiratory tract infection, typically rhinitis and cough. In viral pneu monia, fever is usually
present; temperatures are generally lower than in bacterial pneumonia. Tachypnea is the most
consistent clinical manifestation of pneumonia. Increased work of breathing accompanied by
intercostal, subcostal, and suprasternal retractions, nasal flaring, and use of accessory muscles
is common. Severe infection may be accompanied by cyanosis and respiratory fatigue,
especially in infants. Auscultation of the chest may reveal crackles and wheezing, but it is
often difficult to localize the source of these adventitious sounds in very young children with
hyperresonant chests. It is often not possible to distinguish viral pneumonia clinically from
disease caused by Mycoplasma and other bacterial pathogens.
Bacterial pneumonia in adults and older children typically begins suddenly with a shaking
chill followed by a high fever, cough, and chest pain. In older children and adolescents, a
brief upper respiratory tract illness is followed by the abrupt onset of shaking chills and high
fever accompanied by drowsiness with intermittent periods of restlessness; rapid respirations;
a dry, hacking, unproductive cough; anxiety; and, occasionally, delirium. Circumoral
cyanosis may be observed. Many children are noted to be splinting on the affected side to
minimize pleuritic pain and improve ventilation; they may lie on their side with their knees
drawn up to their chest.
Physical findings depend on the stage of pneumonia. Early in the course of illness,
diminished breath sounds, scattered crackles, and rhonchi are commonly heard over the
affected lung field. With the development of increasing consolidation or complications of
pneumonia such as effusion, empyema, or pyopneumothorax, dullness on percussion is noted
and breath sounds may be diminished. A lag in respiratory excursion often occurs on the
affected side. Abdominal distention may be prominent because of gastric dilation from
swallowed air or ileus. Abdominal pain is common in lower lobe pneumonia. The liver may
seem enlarged because of downward displacement of the diaphragm secondary to
hyperinflation of the lungs or superimposed congestive heart failure. Nuchal rigidity, in the
absence of meningitis, may also be prominent, especially with involvement of the right upper
lobe.
Symptoms described in adults with pneumococcal pneumonia may be noted in older children
but are rarely observed in infants and young children, in whom the clinical pattern is
considerably more variable. In infants, there may be a prodrome of upper respiratory tract
infection and diminished appetite, leading to the abrupt onset of fever, restlessness,
apprehension, and respiratory distress. These infants appear ill with respiratory distress
manifested by grunting; nasal flaring; retractions of the supraclavicular, intercostal, and
subcostal areas; tachypnea; tachycardia; air hunger; and often cyanosis. Results of physical
examination may be misleading, particularly in young infants, with meager findings
disproportionate to the degree of tachypnea. Some infants with bacterial pneumonia may
have associated gastrointestinal disturbances characterized by vomiting, anorexia, diarrhea,
and abdominal distention secondary to a paralytic ileus. Rapid progression of symptoms is
characteristic in the most severe cases of bacterial pneumonia
DIAGNOSIS.
The chest radiograph confirms the diagnosis of pneumonia and may indicate a complication
such as a pleural effusion or empyema. Viral pneumonia is usually characterized by
hyperinflation with bilateral interstitial infiltrates and peribronchial cuffing ( Fig. 397-1 ).
Confluent lobar consolidation is typically seen with pneumococcal pneumonia ( Fig. 397-2 ).
The radiographic appearance alone is not diagnostic and other clinical features must be
considered. Repeat chest x-rays are not required for proof of cure for patients with
uncomplicated pneumonia.
The peripheral white blood cell (WBC) count can be useful in differentiating viral from
bacterial pneumonia. In viral pneumonia, the WBC count can be normal or elevated but is
usually not higher than 20,000/mm
3
, with a lymphocyte predominance. Bacterial pneumonia
(occasionally, adenovirus pneumonia) is often associated with an elevated WBC count in the
range of 15,000-40,000/mm
3
and a predominance of granulocytes. A large pleural effusion,
lobar consolidation, and a high fever at the onset of the illness are also suggestive of a
bacterial etiology. Atypical pneumonia due to C. pneumoniae or M. pneumoniae is difficult
to distinguish from pneumococcal pneumonia by x-ray and other labs, and although
pneumococcal pneumonia is associated with a higher WBC count, erythrocyte sedimentation
rate (ESR), and Creactive protein (CRP), there is considerable overlap.
The definitive diagnosis of a viral infection rests on the isolation of a virus or detection of the
viral genome or antigen in respiratory tract secretions. Growth of respiratory viruses in tissue
culture usually requires 510 days. Reliable DNA or RNA tests for the rapid detection of
RSV, parainfluenza, influenza, and adenoviruses are available and accurate. Serologic
techniques can also be used to diagnose a recent respiratory viral infection but generally
require testing of acute and convalescent serum samples for a rise in antibodies to a specific
viral agent. This diagnostic technique is laborious, slow, and not generally clinically useful
because the infection usually resolves by the time it is confirmed serologically. Serologic
testing may be valuable as an epidemiologic tool to define the incidence and prevalence of
the various respiratory viral pathogens.
The definitive diagnosis of a bacterial infection requires isolation of an organism from the
blood, pleural fluid, or lung. Culture of sputum is of little value in the diagnosis of
pneumonia in young children. Blood cultures are positive in only 10% of children with
pneumococcal pneumonia. In M. pneumoniae infections, cold agglutinins at titers >1 : 64 are
found in the blood in 50% of patients. Cold agglutinins are nonspecific, however, because
other pathogens such as influenza viruses may also cause increases. Acute infection caused
by M. pneumoniae can be diagnosed on the basis of a positive PCR test or seroconversion in
an IgG assay. Serologic evidence such as the anti-streptolysin O (ASO) titer may be useful in
the diagnosis of group A streptococcal pneumonia
Atelektasis
Definition
Atelectasis is a collapse in part of the lungs. Normally, air passes through the airways into small sacs
of the lungs. Oxygen from the air passes through these sacs into the blood. Carbon dioxide also
passes from the blood to the sacs to leave the body. With atelectasis, these sacs are collapsed.
Oxygen and carbon dioxide cannot pass through the collapsed sacs.
A collapse over large areas of the lungs can lead to serious problems. In infants, atelectasis may be:
Congenitalpresent at birth
Blockage in airwaysas a result of an inhaled stool during birth, inhaled object, or a mucus plug
that keeps air from moving into sacs
Lung infectionsmay cause fluid build-up that blocks air to lung sacs
Lack of surfactant (common in premature infants)surfactant is a fluid that lines the inside of the
lungs and helps them function properly
Impaired breathingair is not pulled deep enough into the lungs to open all sacs
Damage to nerve and muscles that control breathingmay prevent coughing, deep breathing, or
yawning
*
Risk Factors
Factors that increase the chance of congenital atelectasis include:
Premature birth
Having anesthesia
Rapid breathing
Agitation
Coughing
Wheezing
Fever