PNEUMONIA

Pneumonia is an acute inflammation of the lung parenchyma caused by a microbial organism.

Risk Factors

Aging.

Air pollution.

Altered consciousness: alcoholism; head injury, seizures, anesthesia, drug overdose, stroke.

Altered oropharyngeal flora secondary to antibiotics.

Bed rest and prolonged immobility.

Chronic diseases: chronic lung disease, diabetes mellitus, heart disease, cancer, end-stage
renal disease. Debilitating illness.

Human immunodeficiency virus (HIV) infection.

Immunosuppressive drugs (corticosteroids, cancer chemotherapy, immunosuppressive

therapy after organ transplant). Inhalation or aspiration of noxious substances.

Intestinal and gastric feedings via nasogastric or nasointestinal tubes.

Malnutrition.

Smoking.

Tracheal intubation (endotracheal intubation, tracheostomy).

Upper respiratory tract infection.

Types of Pneumonia

Bacterial Pneumonia

Bacterial infection of the lung parenchyma is the most common cause of pneumonia or
consolidation of one or both the lungs. Two types of acute bacterial pneumonias are
distinguished—lobar pneumonia and bronchopneumonia (lobular pneumonia), each with
distinct etiologic agent and morphologic changes.
•Pneumococcal pneumonia:

More than 90% of all lobar pneumonias are caused by Streptococcus pneumoniae, a lancet-
shaped diplococcus. Out of various types, type 3-S. pneumoniae causes particularly virulent
form of lobar pneumonia. Pneumococcal pneumonia in majority of cases is community-
acquired infection.

•Staphylococcal pneumonia:

Staphylococcus aureus causes pneumonia by hematogenous spread of infection from another

focus or after viral infections.

•Streptococcal pneumonia

p-hemolytic streptococci may cause pneumonia in severely debilitated elderly patients and in
diabetics.

•Pneumonia by gram-negative aerobic bacteria:

Less common causes of lobar pneumonia are gram-negative bacteria like Haemophilus
influenzae, Klebsiella pneumonia, Pseudomonas, Proteus, Escherichia coli, H. influenzae.

Viral and Mycoplasmal Pneumonia

Viral and mycoplasmal pneumonia is characterised by patchy inflammatory changes, largely

confined to interstitial tissue of the lungs, without any alveolar exudate. Other terms used for
these respiratory tract infections are interstitial pneumonitis, reflecting the interstitial location
of the inflammation, and primary atypical pneumonia, atypicality being the absence of
alveolar exudate commonly present in other pneumonias. Interstitial pneumonitis may occur
in all ages. Most of the cases are mild and transient; exceptionally it may be severe and
fulminant.

Pneumocystis Carinii Pneumonia (PCP)

Pneumocystis carinii, a protozoon widespread in the environment, causes pneumonia by

inhalation of the organisms as an opportunistic infection in neonates and immunosuppressed
people. Almost 100% cases of HFV/AIDS develop opportunistic infection during the course
of disease, most commonly PCP. Other immunosuppressed groups are patients on
chemotherapy for organ transplant and tumors, malnutrition, agammaglobulinemia, etc.

Legionella Pneumonia

Legionella pneumonia or Legionnaire's disease is an epidemic illness caused by gram-

negative bacilli, Legionella pneumophila that thrives in aquatic environment. It was first
recognized following investigation into high mortality among those attending American
Legion Convention in Philadelphia in July, 1976. The epidemic occurs in summer months by
spread of organisms through contaminated drinking water or in air conditioning cooling
towers. Impaired host defenses in the form of immunodeficiency, corticosteroid therapy, old
age and cigarette smoking play important roles.

Aspiration (Inhaiation) Pneumonia

Aspiration or inhalation pneumonia results from inhalation of different agents into the lungs.
These substances include food, gastric contents, foreign body and infected material from oral
cavity. A number of factors predispose to inhalation pneumonia which includes:
unconsciousness, drunkenness, neurological disorders affecting swallowing, drowning,
necrotic oropharyngeal tumors. Some patients die immediately from asphyxiation or
laryngospasm without developing pneumonia.

Hypostatic Pneumonia

Hypostatic pneumonia is the term used for collection of edema fluid and secretions in the
dependent parts of the lungs in severely debilitated, bed-ridden patients. The accumulated
fluid in the basal zone and posterior part of lungs gets infected by bacteria from the upper
respiratory tract and sets in bacterial pneumonia. Hypostatic pneumonia is a common
terminal event in the old, feeble, comatose patients.

Lipid Pneumonia

Another variety of non-infective pneumonia is lipid pneumonia which is of 2 types—

exogenous and endogenous.

1. Exogenous lipid pneumonia: This is caused by aspiration of a variety of oily

materials. These are inhalation of oily nasal drops, regurgitation of oily medicines from
stomach (e.g. liquid paraffin), administration of oily vitamin preparation to debilitated old
patients.

2. Endogenous lipid pneumonia: Endogenous origin of lipids causing pneumonic

consolidation is more common. The sources of origin are tissue breakdown following
obstruction to airways, e.g. obstruction by bronchogenic cancer, tuberculosis and
bronchiectasis.

Lobar Pneumonia

It is an acute bacterial infection of a part of a lobe, the entire lobe, or even two lobes of one or
both the lungs. The common organisms responsible for lobar pneumonia are Staphylococcal
pneumonia, Pneumococcal pneumonia, Streptococcal pneumonia. Hemophilus influenzae,
Klebsiella pneumonia (Friedlander's bacillus), Pseudomonas, Proteus and Escherichia coli, H.
influenza.

Bronchopneumonia (Lobuiar Pneumonia)

Bronchopneumonia or lobular pneumonia is infection of the terminal bronchioles that extends

into the surrounding alveoli resulting in patchy consolidation of the lung. The condition is
particularly frequent at the extremes of life as a terminal event in chronic debilitating diseases
and as a secondary infection following viral respiratory infections such as influenza, measles,
etc. The common organisms responsible for bronchopneumonia are staphylococci,
streptococci, pneumococci, Klebsiella pneumoniae. Hemophilus influenzae, and gram-
negative bacilli like Pseudomonas and coliform bacteria.

Community-acquired pneumonia (CAP) is defined as a lower respiratory tract infection of the

lung parenchyma with onset in the community or during the first 2 days of hospitalization.
The common organisms responsible for CAP are Streptococcus pneumonia. Mycoplasma
pneumonia, Haemophilus influenza. Chlamydia pneumonia, Legionella pneumophila,
Moraxella catarrhalis, Staphylococcus aureus, Nocardia, Enteric aerobic gram-negative
bacteria (e.g. Klebsiella), Fungi, Mycobacterium tuberculosis.

Hospital-acquired pneumonia (HAP) is pneumonia occurring 48 hours or longer after hospital

admission and not incubating at the time of hospitalization. Ventilator-associated pneumonia
(VAP) refers to pneumonia that occurs more than 48 to 72 hours after endotracheal
intubation. The common organisms responsible for HAP are Pseudomonas aeruginosa,
Enterobacter, Escherichia coli, Proteus, Klebsiella, Staphylococcus aureus. Streptococcus
pneumonia.

Pathogenesis

The microorganisms gain entry into the lungs by one of the following four routes:

1. Inhalation of the microbes present in the air.

2. Aspiration of organisms from the nasopharynx or oropharynx.

3. Hematogenous spread from a distant focus of infection.

4. Direct spread from an adjoining site of infection.

The normal lung is free of bacteria because of the presence of a number of lung defense
mechanisms at different

levels such as nasopharyngeal filtering action, mucociliary action of the lower respiratory
airways, the presence of

phagocytosing alveolar macrophages and immunoglobulins. Failure of these defense

mechanisms and presence of

certain predisposing factors result in pneumonias. These conditions are as under:

• Altered consciousness: The oropharyngeal contents may be aspirated in states causing

unconsciousness, e.g. in coma, cranial trauma, seizures, cerebrovascular accidents, drug
overdose, alcoholism, etc.

• Depressed cough and glottic reflexes: Depression of effective cough may allow
aspiration of gastric contents e.g. in old age, pain from trauma or thoracoabdominal surgery,
neuromuscular disease, weakness due to malnutrition, kyphoscoliosis, severe obstructive
pulmonary diseases, endotracheal intubation and tracheostomy.

• Impaired mucociliary transport: The normal protection offered by mucus-covered

ciliated epithelium in the airways from the larynx to the terminal bronchioles is impaired or
destroyed in many conditions favoring passage of bacteria into the lung parenchyma. These
conditions are cigarette smoking, viral respiratory infections, immotile cilia syndrome,
inhalation of hot or corrosive gases and old age.
• Impaired alveolar macrophagefunction: Pneumonias may occur when alveolar
macrophage function is impaired, e.g. by cigarette smoke, hypoxia, starvation, anemia,
pulmonary edema and viral respiratory infections.

• Endobronchial obstruction: The effective clearance mechanism is interfered in

endobronchial obstruction from tumor, foreign body, cystic fibrosis and chronic bronchitis.

• Leucocyte dysfunctions: Disorders of lymphocytes including congenital and acquired

immunodeficiencies (e.g. AIDS, immunosuppressive therapy) and granulocyte abnormalities
may predispose to pneumonia.

Pathophysiology

Congestion

After the pneumococcus organisms reach the alveoli, there is an outpouring of fluid into the
alveoli. The organisms multiply in the serous fluid, and the infection is spread. The
pneumococci damage the host by their overwhelming growth and by interfering with lung
function.

Red Hepatization

There is massive dilation of the capillaries, and alveoli are filled with organisms, neutrophils,
red blood cells (RBCs), and fibrin. The lung appears red and granular, similar to the liver, this
is why the process is called red hepatization.

Gray Hepatization

Blood flow decreases, and leukocytes and fibrin consolidate in the affected part of the lung

Resolution

Complete resolution and healing occur if there are no complications. The exudate becomes
lysed and is processed by the macrophages. The normal lung tissue is restored, and the
person's gas-exchange ability returns to normal.

Clinical Manifestations

Patients with pneumonia usually have a sudden onset of symptoms, including fever, shaking
chills, shortness of breath, cough productive of purulent sputum (rust-colored sputum can be
seen in pneumococcal pneumonia), and pleuritic chest pain (in some cases). In the elderly or
debilitated patient, confusion or stupor (possibly related to hypoxia) may be the only finding.
On physical examination, signs of pulmonary consolidation, such as dullness to percussion,
increased fremitus, bronchial breath sounds, and crackles, may be found. The typical
pneumonia syndrome is usually caused by the most common pathogen, S. pneumoniae, but
can also be due to other bacterial pathogens, such as H. influenzae.

Pneumonia may also manifest atypically with a more gradual onset, a dry cough, and
extrapulmonary manifestations such as headache, myalgias, fatigue, sore throat, nausea,
vomiting, and diarrhea. On physical examination, crackles are often heard. This presentation
of manifestations is classically produced by M. pneumoniae but can also be caused by
Legionella and C. pneumoniae.

The initial manifestations of viral pneumonia are highly variable. Viruses also cause
pneumonia that is usually characterized by an atypical presentation with chills, fever, dry,
nonproductive cough, and extrapulmonary symptoms. Primary viral pneumonia can be
caused by influenza virus infection. Viral pneumonia is also found in association with
systemic viral diseases such as measles, varicella-zoster, and herpes simplex.

Complications

Pleurisy •

Atelectasis •

Lung abscess •

Pericarditis •

Endocarditis

Diagnostic Studies

The diagnosis of pneumonia is made by history (particularly of a recent respiratory tract

infection), physical examination, chest X-ray studies, blood culture (bloodstream invasion,
called bacteremia, occurs frequently), and sputum examination. Invasive procedures may be
used to collect specimens. Sputum may be obtained by nasotracheal or orotracheal suctioning
with a sputum trap or by fiberoptic bronchoscopy. Bronchoscopy is often used in patients
with acute severe infection, patients with chronic or refractory infection, or
immunocompromised patients when a diagnosis cannot be made from an expectorated or
induced specimen.

Management

Uncomplicated Community Acquired Pneumonia

• Amoxicillin 500 mg 8-hourly orally ^

• If patient is allergic to penicillin

- Clarithromycin 500 mg 12-hourly orally

- Erythromycin 500 mg 6-hourly orally.

• If Staphylococcus is cultured or suspected

- Flucloxacillin 1-2 g 6-hourly IV

- Clarithromycin 500 mg 12-hourly IV.

• If Mycoplasma or Legionella is suspected

- Clarithromycin 500 mg 12-hourly orally or IV

- Erythromycin 500 mg 6-hourly orally or IV

- Rifampicin 600 mg 12-hourly i.v. in severe cases.

Severe Community Acquired Pneumonia

Clarithromycin 500 mg 12-hourly IV

Erythromycin 500 mg 6-hourly FV Co-amoxiclav 1.2 g 8-hourly IV Ceftriaxone 1-2 g daily

IV.

Cefuroxime 1.5 g 8-hourly IV Amoxicillin 1 g 6-hourly FV Flucloxacillin 2 g 6-hourly IV.

Hospital Acquired Pneumonia

Patients without risk factors for multi drug resistance

• Ceftriaxone (2 g FV q24h)
• Moxifloxacin (400 mg FV q24h), ciprofloxacin (400 mg FV q8h), levofloxacin (750
mg IV q24h)

• Ampicillin/Sulbactam (3 g IV q6h)

• Ertapenem (1 g FV q24h).

Patients with risk factors for multi drug resistance A-lactam:

• Ceftazidime (2 g IV q8h) or Cefepime (2 g IV q8-12h)

• Piperacillin/Tazobactam (4.5 g IV q6h); Imipenem (500 mg IV q6h or 1 g IV q8h), or

Meropenem (1 g IV q8h). Antibiotics active against gram-negative bacteria

• Gentamicin or tobramycin (7 mg/kg IV q24h) or amikacin (20 mg/kg IV q24h)

• Ciprofloxacin (400 mg IV q8h) or levofloxacin (750 mg IV q24h).

Antibiotics active against gram-positive bacteria

• Linezolid (600 mg IV ql2h)

• Vancomycin (15 mg/kg, up to 1 g FV, ql2h).

Nursing Interventions

Improving Gas Exchange

Observe for cyanosis, dyspnea, hypoxia, and confusion, indicating worsening condition.

Follow ABG levels/SaO^ to determine oxygen need and response to oxygen therapy.

Administer oxygen at concentration to maintain Pa02 at acceptable level. Hypoxemia maybe

encountered because of abnormal ventilation-perfusion ratios in affected lung segments.

Avoid high concentrations of oxygen in patients with COPD, particularly with evidence of
CO2 retention; use of high oxygen concentrations may worsen alveolar ventilation by
depressing the patient's only remaining ventilatory drive. If high concentrations of oxygen are
given, monitor alertness and PaO^ and Pac02 levels for signs of CO2 retention. Place patient
in an upright position to obtain greater lung expansion and improve aeration. Frequent
turning and increased activity (up in chair, ambulate as tolerated) should be employed.
Enhancing Airway Clearance

Obtain freshly expectorated sputum for gram-stain and culture, preferably early morning
specimen as directed. Instruct the patient as follows:

• Encourage patient to cough; retained secretions interfere with gas exchange. Suction
as necessary.

• Encourage increased fluid intake, unless contraindicated, to thin mucus and promote
expectoration and replace fluid losses caused by fever, diaphoresis, dehydration, and
dyspnea.

• Humidify air or oxygen therapy to loosen secretions and improve ventilation.

• Employ chest wall percussion and postural drainage when appropriate to loosen and
mobilize secretions.

• Auscultate the chest for crackles and rhonchi.

Administer cough suppressants when coughing is nonproductive only if there is no evidence

of retained secretions. Mobilize patient to improve secretion clearance and reduce risk of
atelectasis and worsening pneumonia.

Relieving Pleuritic Pain

• Place in a comfortable position (semi-Fowler's) for resting and breathing; encourage

frequent change of position to prevent pooling of secretions in lungs.

• Demonstrate how to splint the chest while coughing.

• Avoid suppressing a productive cough.

• Administer prescribed analgesic agent to relieve pain. Avoid opioids in patients with a
history of COPD.

• Apply heat and/or cold to chest as prescribed.

• Assist with intercostal nerve block for pain relief.

• Encourage modified bed rest during febrile period.

• Watch for abdominal distention or ileus, which may be due to swallowing of air
during intervals of severe dyspnea. Insert a nasogastric (NG) or rectal tube as directed.

Promoting Rest and Conserving Energy

The nurse encourages the debilitated patient to rest and avoid overexertion and possible
exacerbation of symptoms. The patient should assume a comfortable position to promote rest
and breathing (e.g. semi-Fowler's) and should change