NARRATIVE PATHOPHYSIOLOGY OF PNEUMONIA

Bacteria commonly enter the lower airways but do not normally cause pneumonia because of extensive defense mechanism. But with the immature defense mechanism of infants, they are more susceptible to these invading organisms that may cause pneumonia. Bacteria reach the lung by one of the four routes: inhalation from the ambient air, aspiration from the previously colonized upper airway, direct spread from contiguous infected sites, or hematogenous spread. After bacteria reach the lower airways from the ineffective host defenses on the upper respiratory tract, they encounter a number of host defenses for the second time that prevent them from entering the lung and causing pneumonia. A localized inflammation occur as the body fights off with the invading microorganisms that is evidenced by an increase in the WBC count, increase mucus production that could obstruct the airway if excessive mucus is produced, and weakness of the patient as energy is used up to counter act the invading microorganisms. An impaired or weak immune defenses predispose to colonization and infection of the lower respiratory system. Immune defenses include the bronchial-associated lymphoid tissue, phagocytic cells, immunoglobulins, and T-cell-mediated cellular immunity. Bacterial adherence also plays a role in colonization of the lower airways. The epithelial cells of critically and chronically ill persons are more receptive to binding microorganisms that cause pneumonia. Another clinical risk factor favoring colonization of the tracheobronchial tree include antibiotic therapy that alters the normal bacterial flora. Bacterial pneumonia results from the infection by bacteria that multiply extracellularly in the alveoli and cause inflammation and exudation of fluid into the air-filled spaces of the alveoli, as evidenced by crackles upon auscultation on lung fields. As the infection reaches the alveoli,

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the patient will experience a productive cough, restlessness from shortness of breath as excessive production of secretions may obstruct the airways that could lead to tachycardia, nasal flaring and use of accessory muscles upon breathing to compensate with the bodys need for oxygen. If this infection is not treated, this could lead to certain lung complications like empyema, lung abscess, pleurisy, and pericarditis. Chest thoracostomy tube insertion may be necessary if severe pulmonary edema occurs.

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PATHOPHYSIOLOGY OF PNEUMONIA
Predisposing factors

Age (1 month vulnerable group) Previous hospitalization (sepsis neonaturum ) Immobilization Previous antibiotic therapy that may have destroyed normal bacterial flora Mixed feeding

Precipitating factors

Exposure and infection from unknown bacteria through inhalation of contaminated air breathed

Invasion of exceeding virulent bacteria through inhalation of air

Organism reach upper respiratory airway

Ineffective defense mechanism

Organism reaches lower airway

Encounter with a number of host defenses Increased WBC count (14,000); weakness

Occurrence of localized inflammation

Increased mucus production Tachycardia(184bp m); paleness; shallow breathing; use of accessory muscles on breathing and nasal flaring

Yellowish secretions; nasal flaring

Ventilation decreases

Altered defenses from weak immune system

Bacteria invades alveolar cells in the lungs Productive cough; SOB; shallow breathing;restlessness

Bacteria multiply extracellularly into the alveoli

Increased WBC count (14,000) and general weakness

Inflammation of lungs

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CXR result: Blotchy densities on inner and midlung zones

Exudation of fluid into air-filled spaces of the alveoli

Crackling breath sounds; SOB

PNEUMONIA

Pulmonary edema

If untreated:  Empyema  Lung Abscess  Pleurisy  Pericarditis

If treated: Return to normal breathing pattern, respiratory rate within 3080cpm and absence of adventitious breath sounds

DEATH

LEGEND: Predisposing Factors Precipitating factors

Disease process

Signs

Chest X-Ray result (Lab)

Complications

Effects when treated

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