Pneumonia

An infection of the pulmonary parenchyma

Classified as CAP, HAP, VAP, and HCAP
Proliferation of microbial pathogens at the alveolar level and the hosts
response to those pathogens
Microorganisms gain access to the lower respiratory tract in several ways
o Aspiration from the oropharynx
o Hematogenous spread
o Contiguous extension from an infected pleural or mediastinal space
Hosts defense
o Hairs and turbinates capture larger inhaled particles before they reach
the lower respiratory tract
o Branching architecture of tracheo-bronchial tree traps microbes on the
airway lining where mucociliary clearance and local antibacterial
factors clear/kill the potential pathogen
o Gag reflex and cough mechanism are critical protection from aspiration
o Normal flora adhering to the mucosal cells of the oropharynx, whose
components are remarkably constant, prevents pathogenic bacteria
from binding and therey decreases risk of pneumonia caused by these
more virulent bacteria
When these barriers are overcome, or microorganisms are small enough to be
inhaled to the alveolar level, resident alveolar macrophages are extremely
efficient at clearing and killing pathogens. They are assisted by proteins that
are produced by the alveolar epithelial cells (surfactant proteins A and D) that
have opsonizing properties or antibacterial/viral activity
o Once engulfed by the macrophage, the pathogens are eliminated via
either the mucociliary elevator or the lymphatics and has no more risk
for infection
o When the capacity of the alveolar macrophages to ingest or kill the
microorganisms is exceeded does clinical pneumonia become
manifest. Then the alcveolar macrophages initiate the inflammatory
response to bolster the lower respiratory tract defenses
The hosts inflammatory response (rather than proliferation of pathogen),
triggers the clinical syndrome of pneumonia.
o Release of inflammatory mediators such as interleukin 1 and tumor
necrosis factor results in fever
o Chemokines (interleukin 8 and granulocyte colony-stimulating factor)
stimulates the release of neutrophils and their attraction to the lung
producing peripheral leukocytosis and purulent secretions
o Inflammatory mediators released by macrophages and neutrophils
create an alveolar capillary leak equivalent to that seen in the ARDS
just localized (even erythrocytes can cross the alveolar capillary
membrane causing hemoptysis)
Capillary leak results in radiographic infiltrate and rales
detectable on auscultation and hypoxemia results from alveolar
filling

Hypoxemic vasoconstriction occurring normally in fluid-filled

alveoli can be interfered by some pathogens resulting to severe
anemia
Increased respiratory drive in systemic inflammatory response
syndrome leads to respiratory alkalosis

*decreased compliance due to capillary leak, hypoxemia, increased respiratory

drive, increased secretions, and occasionally infection-related bronchospasm all
lead to dyspnea. If severe enough, the changes in lung mechanism secondary to
reductions in lung volume and compliance and the intrapulmonary shunting of blood
may cause respiratory failure and death
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Pathology (classic pneumonia) Phases (lobar pneumococcal pneumonia)

o Edema phase - exudate
o Red Hepatization phase erythrocytes and bacteria in exudate
o Gray Hepatization phase no new erythrocytes, previous erythrocytes
have been lysed and degraded, neutrophil is the predominant cell,
fibrin deposition is abundant, bacteria have disappeared
o Resolution phase macrophage reappears as the dominant cell in the
alveolar space, debris of the battle and the inflammatory response has
been cleared
Treatment
o Antibiotics. These medicines are used to treat bacterial pneumonia. It
may take time to identify the type of bacteria causing your pneumonia
and to choose the best antibiotic to treat it. If your symptoms don't
improve, your doctor may recommend a different antibiotic.
o Cough medicine. This medicine may be used to calm your cough so
that you can rest. Because coughing helps loosen and move fluid from
your lungs, it's a good idea not to eliminate your cough completely. In
addition, you should know that very few studies have looked at
whether over-the-counter cough medicines lessen coughing caused by
pneumonia. If you want to try a cough suppressant, use the lowest
dose that helps you rest.
o Fever reducers/pain relievers. You may take these as needed for fever
and discomfort. These include drugs such as aspirin, ibuprofen (Advil,
Motrin IB, others) and acetaminophen (Tylenol, others).

Acute respiratory distress syndromeif ukkbess

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Clinical syndrome of severe dyspnea of rapid onset, hypoxemia, and diffuse

pulmonary infiltrates leading to respiratory failure
Caused by diffuse lung injury from many underlying medical and surgical
disorders
o Lung injury- toxic inhalation (direct), sepsis (indirect)
Clinical Course and Pathophysiology
o Exudative Phase
Encompasses 1st 7 days of illness after exposure to ARDS risk
factor
Alveolar capillary endothelial cells and type I pneumocytes
(alveolar epithelial cells) are injured with consequent loss of the
normally tight alveolar barrier to fluid and macromolecules
Edema fluid rich in protein accumulates in the interstitial and
alveolar spaces
Cytokines and lipid mediators present in the lung migration of
leukocytes
Condensed plasma proteins aggregate in the air spaces with
cellular debris and dysfunctional pulmonary surfactant to form
hyaline membrane whorls
Alveolar edema involves dependent portions of the lung, with
diminished aeration and collapse decreased lung compliance
Intrapulmonary shunting and hypoxemia develop increased
work of breathing dyspnea
Microvascular occlusions results in reduction of pulmonary blood
flow to ventilated portions of the lung and pulmonary
hypertension
o Proliferative Phase
Day 7-21
Most patients recover rapidly and are liberated from mechanical
ventilation during this phase
Signs of resolution (histologically): Initiation of lung repair,
organization of alveolar exudates, shift from neutrophil
predominant lymphocyte predominant pulmonary infiltrate,
type II pneumocytes proliferate along alveolar basement
membranes to synthesize new pulmonary surfactant and
differentiate into type I pnuemocytes
Dyspnea, tachypnea, hypoxemia may still be present
Some may develop progressive lung injury and early changes of
pulmonary fibrosis
o Fibrotic Phase
If the patient did not recover after 3-4 weeks after pulmonary
injury, his respiratory tract enters the fibrotic phase
May require long-term support on mechanical ventilators and/or
supplemental oxygen

Histologically: alveolar edema and inflammatory exudates or

earlier phases are now converted to extensive alveolar-duct and
interstitial fibrosis
Marked disruption of acinar architecture leads to emphysemalike changes, with large bullae
Intimal fibroproliferation in the pulmonary microcirculation
causes progressive vascular occlusion and pulmonary
hypertension increased risk of pneumothorax, reductions in
lung compliance, increased pulmonary dead space
Substantial burden of excess morbidity

Treatment
o Critically ill patient care. Requires close attention to
The recognition and treatment of underlying medical and
surgical disorders (sepsis, aspiration, trauma)
The minimization of procedures and their complications
Prophylaxis against venous thrombo-embolism, GI bleeding,
aspiration, excessive sedation, central venous catherte
infections
Prompt recognition of nosocomial infections
Provision of adequate nutrition