This lecture is supposed to ease approach to pneumonia for healthcare professionals who are at work and in training

1. Melaku Yitbarek(M.D)
Internal Medicine Unit,
March 2018

2. • Definition
• Pathophysiology
• Classification
• Clinical features
• Treatment
• Complications
• Prevention

3. Pneumonia is an infection of the
pulmonary parenchyma.
Despite being the cause of significant
morbidity and mortality, pneumonia is often
misdiagnosed, mistreated, and
underestimated

4.  Pneumonia results from the proliferation of microbial
pathogens at the alveolar level and the host’s response to
those pathogens.
 Microorganisms gain access to the lower respiratory tract in
several ways, the most common is by aspiration from the
oropharynx.
 Small-volume aspiration occurs frequently during sleep
(especially in the elderly) and in patients with decreased levels
of consciousness.
 Many pathogens are inhaled as contaminated droplets.
 Rarely,pneumonia occurs via hematogenous spread (e.g.,
from tricuspid endocarditis)or by contiguous extension from an
infected pleural or Mediastinal space.

5.  Mechanical factors are critically important in host
defense.
 The hairs and turbinates of the nares capture
larger inhaled particles before they reach the lower
respiratory tract.
 The branching architecture of the tracheobronchial
tree traps microbes on the airway lining,where
mucociliary clearance and local antibacterial
factors either clear or kill the potential pathogen.
 The gag reflex and the cough mechanism offer
critical protection from aspiration.

6.  When these barriers are overcome or when microorganisms are
small enough to be inhaled to the alveolar level, resident alveolar
macrophages are extremely efficient at clearing and killing
pathogens.
 Macrophages are assisted by proteins that are produced by the
alveolar epithelial cells (e.g., surfactant proteins A and D) and that
have intrinsic opsonizing properties or antibacterial or antiviral
activity.
 Once engulfed by the macrophage, the pathogens—even if they are
not killed—are eliminated via either the mucociliary elevator or the
lymphatics and no longer represent an infectious challenge.
 Only when The capacity of the alveolar macrophages to ingest or kill
the Microorganisms is exceedes does clinical pneumonia become
manifest

7.  In that situation, the alveolar macrophages initiate the
inflammatory response to bolster lower respiratory tract
defenses
 The release of inflammatory mediators, such as interleukin 1
and tumor necrosis factor, results in fever.
 Chemokines,such as interleukin 8 and granulocyte colony-
stimulating factor,stimulate the release of neutrophils and their
attraction to the lung,producing both peripheral leukocytosis
and increased purulent secretions
 Inflammatory mediators released by macrophages and the
Newly recruited neutrophils create an alveolarcapillary leak

8. The capillary leak results in a radiographic
infiltrate and rales detectable on
auscultation, and hypoxemia results from
alveolar filling.
Moreover, some bacterial pathogens
appear to interfere with the hypoxemic
vasoconstriction that would normally occur
with fluid filled alveoli, and this interference
can result in severe hypoxemia.

16. Etiology:
 The extensive list of potential etiologic agents
in CAP includes bacteria, fungi, viruses, and
protozoa
 Most cases of CAP, however, are caused by
relatively few pathogens
 Although Streptococcus pneumoniae is most
common, other organisms also must be
considered in light of the patient’s risk factors
and severity of illness

17. Typical Organisms
 S.pneumoniae,
 Haemophilus influenzae,
 and (in selected patients)
S. aureus
 and gram-negative bacilli
such as
 Klebsiella pneumoniae
and Pseudomonas
aeruginosa
Atypical organisms
 Mycoplasma pneumoniae,
 Chlamydia pneumoniae,
 and Legionella species (in
inpatients) as well as
respiratory viruses
 such as influenza viruses,
adenoviruses, human
metapneumovirus,
 and respiratory syncytial
viruses

18. Epidemiology:
 More than 5 million CAP cases occur annually in the
United States;
 usually, 80% of the affected patients are treated as
outpatients and 20% as inpatients.
 The mortality rate among outpatients is usually <1%,
 whereas among hospitalized patients the rate can
range from ~12%to 40%, depending on whether
treatment is provided in or outside of the intensive care
unit (ICU).
 The incidence rates are highest at the extremes of age

19. Risk factors:
 Risk factors for CAP include alcoholism,
asthma,immunosuppression,institutionalization, and an age of
>70 years
 In the elderly, factors such as decreased cough and gag
reflexes
 Risk factors for pneumococcal pneumonia include dementia,
seizure disorders, heart failure, cerebrovascular disease,
alcoholism, tobacco smoking, chronic obstructive pulmonary
disease, and HIV infection
 P. aeruginosa is a particular problem in patients with severe
structural lung disease, such as bronchiectasis, cystic
fibrosis, or severe chronic obstructive pulmonary disease

20. Clinical Manifestations:
CAP can vary from indolent to fulminant in
presentation and from mild to fatal in
severity.
The clinical presentation may not be so
obvious in the elderly, who may initially
display new-onset or worsening confusion
and few other manifestations

21. Hx:
• Fever
• Cough
• Chest Pain
• Fast breathing
• nausea, vomiting, and/or
diarrhea
• fatigue, headache,
myalgias, and arthralgia
PE:
 An increased respiratory
rate and use of accessory
muscles of respiration
 increased or decreased
tactile fremitus,
 and the percussion note
can vary from dull to flat,
 Crackles, bronchial breath
sounds, and possibly a
pleural friction rub may be
heard on auscultation

22. Diagnosis:
• Clincal: Hx and PE
• Laboratory findings: sputum gram stain
and culture
• Blood culture
• Imaging: Chest x-ray

23. Treatment:
Objectives
 Treat the infection.
 Prevent complications.
Identify those that are at high risk and may require hospitalization.
Ther CURB-65 scoring systems suggested to evaluate the prognosis and
determine subsequent management:
 CURB-65
 C-Confusion=1point
 U-Uremia: BUN >30/dL=1point
 R-RR >30/min= 1point
 BP <90/60=1point
 Age>65=1point
 If score is 1point, it is ok to give outpatient treatment. If the score is greater
than 1 point, the patient needs hospitalization. The higher the score, the
higher the mortality.
Non pharmacologic
 Bed rest
 Adequate hydration

24. Treatment:
Pharmacologic
• Community acquired ambulatory patients (Mild
Pneumonia):First line
 No recent antibiotic use:
 Clarithromycin, 500mg P.O., BID for 5-7 days
OR
 Azitromycin, 500mg P.O., first day then 250mg
P.O., for 4d.
OR
 Doxycycline, 100mg P.O., BID for 7-10 days.

25. Treatment:
If recent antibiotic use within 3months:
 Clarithromycin, 500mg P.O. BID for 5-7 days
OR
 Azitromycin, 500mg P.O first day then 250mg
P.O., for 4d.
PLUS
 Amoxicillin, 1000mg P.O., TID for 5 to 7 days.
OR
 Amoxicillin- clavulanate, 625mg P.O., TID for 5-
7days

26. Treatment:
Community acquired hospitalized patients
(Severe Pneumonia)
Non-pharmacologic
 Bed rest
 Frequent monitoring of temperature, blood
pressure and pulse rate in order to detect
complications early and to monitor response to
therapy.
 Give attention to fluid and nutritional replacements.
 Administer Oxygen via nasal prongs or face mask

27. Treatment… severe CAP
Pharmacologic
 The Antibiotic choice should be aimed at the most likely
causative agent.
Empiric treatment for pneumonia due to common
organisms:
First line
 Ceftriaxone, 1g I.V. OR I.M every 12-24 hours for 7 days.
OR
 Benzyl penicillin, 2-3 million IU I.V. QID for 7-10 days.
PLUS
 Azithromycin, 500mg on day 1 followed by 250mg/day on
days 2 – 5
OR
 Clarithromycin, 500mg P.O., BID for 7-10 days

28. Complications:
As in other severe infections, common
complications of severe CAP include:
• respiratory failure,
• shock and
• multi organ failure,
• coagulopathy, and exacerbation of comorbid
illnesses.
• Three particularly noteworthy conditions are
metastatic infection, lung abscess,and
complicated pleural effusion

29. Prevention:
• The main preventive measure is
vaccination :influenza and pneumococcal
vaccines
• smokers should be strongly encouraged
to stop smoking

30.  While significantly less well studied than VAP,
HAP in nonintubated patients—both inside
and outside the ICU—is similar to VAP.
 The main differences are the higher
frequency of non-MDR pathogens and the
better underlying host immunity in non
intubated patients.
 The lower frequency of MDR pathogens
allows monotherapy in a larger proportion of
cases of HAP than of VAP

31. Treatment:
Empiric treatment for commonly suspected etiologies of HAP
First line
 Ceftazidime, 1gm I.V. TID for 10-14days
PLUS
 Vancomycin 1g I.V. BID for 10-14 days
OR (particularly in the ICU setup and in ventiltor associated pneumonia)
 Imipenem-cilastatin, 500mg IV (infused slowly over 1hour) Q6h
OR
 Meropenem, 1gm IV (infused slowly over 30min) Q8h
Alternatives
 Ceftriaxone, 1-2g I.V. OR I.M. BID for 7 days.
PLUS
 Gentamicin, 3-5mg/kg I.V. QDdaily in divided doses for 7 days.
OR
 Ciprofloxacin, 500mg P.O./I.V. BID every 12 hours for 7 days.
If methicillin-resistant (MRSA) suspected
 Vancomycin, 1 g I.V. BID should be added to the existing empric
regimen

32.  HCAP represents a transition between classic
CAP and typical HAP
 Several early studies were limited topatients
with culture-positive pneumonia.
 In these studies, the incidence of MDR
pathogens in HCAP was as high as or higher
than in HAP/VAP
 Patients in nursing homes and those who
have recent hospitalization(i.e with in 90
days) are at higher risk

33. Potential etiologic agents of VAP include
both MDR and non-MDR bacterial
pathogens
Most hospitals have problems with
P.aeruginosa and MRSA
Less commonly, fungal and viral
pathogens cause VAP, usually affecting
severely immunocompromised patients.

34. • Harrison’s Principles of Internal
Medicine,19th Edition,
• Standard Treatment Guideline for general
Hospital,2014
• Uptodate 21.6

35. Thank You…