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Jen Denno RN, BSN, CEN
Pneumonia
 Vaccination
 Percent of adults 65 years and over who had ever received a pneumococcal
vaccination: 59%
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Health Care Use
Hospital inpatient care
Number of discharges: 1.1 million
Average length of stay: 5.2 days
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Nursing home care
Number of residents with pneumonia: 33,700
Percent of residents with pneumonia: 2.3%
Mortality
Number of deaths: 50,774
Deaths per 100,000 population: 16.5
VIRAL
 Viral infections are characterized
by the accumulation of mononuclear cells in the submucosa
 and perivascular space, resulting in partial obstruction
of the airway. Patients with these infections present
with wheezing and crackles.
 Disease progresses when the alveolar type II cells lose
their structural integrity and surfactant production is
diminished, a hyaline membrane forms, and
pulmonary edema develops.
Bacterial
 In bacterial infections, the alveoli fill
with proteinaceous fluid, which
triggers a brisk influx of red blood
cells (RBCs) and polymorphonuclear
(PMN) cells (red hepatization)
followed by the deposition of fibrin
and the degradation of inflammatory
cells (gray hepatization). During
resolution, intra-alveolar debris is
ingested and removed by the alveolar
macrophages. This consolidation leads
to decreased air entry and dullness to
percussion; inflammation in the small
airways leads to crackles.
 Four stages of lobar pneumonia have been described.
 In the first stage, which occurs within 24 hours of
infection, the lung is characterized microscopically by
vascular congestion and alveolar edema. Many bacteria and
few neutrophils are present.
 The stage of red hepatization (2-3 d), so called because of
its similarity to the consistency of liver, is characterized by
the presence of many erythrocytes, neutrophils,
desquamated epithelial cells, and fibrin within the alveoli.
 In the stage of gray hepatization (2-3 d), the lung is graybrown to yellow because of fibrinopurulent exudate,
disintegration of RBCs, and hemosiderin.
 The final stage of resolution is characterized by resorption
and restoration of the pulmonary architecture. Fibrinous
inflammation may lead to resolution or to organization
and pleural adhesions.
 In interstitial pneumonia, patchy or diffuse
inflammation involving the interstitium is
characterized by infiltration of lymphocytes
and macrophages. The alveoli do not
contain a significant exudate, but proteinrich hyaline membranes similar to those
found in adult respiratory distress syndrome
(ARDS) may line the alveolar spaces.
 Bacterial superinfection of viral pneumonia
can also produce a mixed pattern of
interstitial and alveolar airspace
inflammation.
Klebsiella
 How do you get it?
 What does it look like?
 What happens as the condition
 spreads?
 They gain entry into the body by eating unwashed vegetables and drinking
contaminated water.
 Most of the time, a Klebsiella pneumoniae infection is very common in
patients with underlying diseases like diabetes, chronic lung diseases, chronic
alcoholics, etc. It is mostly a nosocomial infection that occurs in hospitalized
patients with weakened immune system.
 Once Klebsiella pneumoniae enters the lungs, it causes many destructive
changes in the lungs. It leads to necrosis, inflammation, hemorrhage, etc. of
the lung tissues. This leads to production of a very thick, jelly like mucus that is
called 'currant jelly sputum'. The rapid destruction of the lung tissues is the
distinguishing factor for Klebsiella pneumoniae infection. Initially, Klebsiella
pneumoniae will cause a sudden high fever. This fever is generally more than
103ºF. The fever is accompanied by other symptoms like chills and dizziness.
The patient will also cough up the thick currant jelly sputum. This sputum may
show streaks of blood.
 As the condition spreads, it leads to formation of abscess. These abscesses are
dead tissue pockets that contain millions of Klebsiella pneumoniae bacteria.
Formation of abscesses cause the lungs to stick with the connective tissues
surrounding them. This may lead to collapsed lungs in some patients. Soon,
the infection spreads to the upper respiratory tract. When the infection
spreads, it causes severe airway congestion. This leads to a foul-smelling nasal
discharge.