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PNEUMONIA
Dr. Firoz A Hakkim
MBBS MD
PULMONARY MEDICINE
• Pneumonia is an infection of the pulmonary
parenchyma.
• caused by acute infection, usually bacterial,
characterized by clinical and/or radiographic
signs of consolidation of a part or parts of one
or both lungs.
• ‘Lobar pneumonia’ is a radiological and
pathological term referring to homogeneous
consolidation of one or more lung lobes, often
with associated pleural inflammation.
• Bronchopneumonia’ refers to more patchy
alveolar consolidation associated with
bronchial and bronchiolar inflammation, often
affecting both lower lobes.
PATHOPHYSIOLOGY
• proliferation of microbial pathogens at the
alveolar level and the host’s response to those
pathogens.
• aspiration from the oropharynx
• Pathogens are inhaled as contaminated
droplets.
• hematogenous spread (e.g., from tricuspid
endocarditis) or by contiguous extension from an
infected pleural or mediastinal space.
• Once engulfed, the pathogens—even if they are
not killed by macrophages—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and no longer represent an infectious challenge.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 exceeded does clinical pneumonia become
manifest.
• Alveolar macrophages initiate the
inflammatory response to bolster lower
respiratory tract defenses.
• Inflammatory mediators released by
macrophages and the newly recruited
neutrophils create an alveolar capillary leak.
• The capillary leak results in a radiographic
infiltrate and rales detectable on auscultation,
and hypoxemia results from alveolar filling.
PATHOLOGY
• Edema
• red hepatization
• gray hepatization
• resolution
• Edema- with the presence of a proteinaceous
exudate - and often of bacteria—in the alveoli.
• This phase is rarely evident in clinical or
autopsy specimens because it is so rapidly
followed by a red hepatization phase.
• red hepatization - presence of erythrocytes in
the cellular intraalveolar exudate gives this
second stage its name, but neutrophils are
also present and are important from the
standpoint of host defense.
• Bacteria are occasionally seen in cultures of
alveolar specimens collected during this
phase.
• gray hepatization - no new erythrocytes are
extravasating, and those already present have
been lysed and degraded.
• The neutrophil is the predominant cell, fibrin
deposition is abundant, and bacteria have
disappeared.
• This phase corresponds with successful
containment of the infection and
improvement in gas exchange.
• Resolution - the macrophage is the dominant
cell type in the alveolar space, and the debris
of neutrophils, bacteria, and fibrin has been
cleared, as has the inflammatory response.
COMMUNITY-ACQUIRED
PNEUMONIA
• extensive list of potential etiologic agents in
CAP includes bacteria, fungi, viruses, and
protozoa.
• Clinical features – patient is frequently febrile,
with a tachycardic response, and may have
chills and/or sweats and cough that is either
nonproductive or productive of mucoid,
purulent, or blood-tinged sputum.
• Pleuritic chest pain, gastrointestinal symptoms
• increased respiratory rate, use of accessory
muscles of respiration.
• Palpation may reveal increased or decreased
tactile fremitus
• percussion note can vary from dull to flat,
reflecting underlying consolidated lung and
pleural fluid.
• Crackles, bronchial breath sounds, and
possibly a pleural friction rub may be heard on
auscultation.
Pa view
Lateral view
Management
• Oxygen should be administered to all patients
with tachypnoea, hypoxaemia, hypotension or
acidosis, with the aim of maintaining the PaO2
at or above 8 kPa (60 mmHg) or the SaO2 at
or above 92%.
• Intravenous fluids – severe illness, older
patients and those who are vomiting.
Inotropic support may be required in patients
with shock.
Discharge and follow-up
• depends on their home circumstances and the
likelihood of complications.
• Clinical review should be arranged around 6
weeks later and a chest X-ray obtained if there
are persistent symptoms, physical signs or
reasons to suspect underlying malignancy.
Prevention
• Current smokers should be advised to stop.
• Influenza and pneumococcal vaccination.
• Tackling malnourishment and indoor air
pollution, and encouraging immunisation
against measles, pertussis and Haemophilus
influenzae type b are particularly important in
children.
THANK YOU

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Pneumonia

  • 1. PNEUMONIA Dr. Firoz A Hakkim MBBS MD PULMONARY MEDICINE
  • 2.
  • 3. • Pneumonia is an infection of the pulmonary parenchyma. • caused by acute infection, usually bacterial, characterized by clinical and/or radiographic signs of consolidation of a part or parts of one or both lungs.
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  • 7. • ‘Lobar pneumonia’ is a radiological and pathological term referring to homogeneous consolidation of one or more lung lobes, often with associated pleural inflammation. • Bronchopneumonia’ refers to more patchy alveolar consolidation associated with bronchial and bronchiolar inflammation, often affecting both lower lobes.
  • 8.
  • 9. PATHOPHYSIOLOGY • proliferation of microbial pathogens at the alveolar level and the host’s response to those pathogens. • aspiration from the oropharynx • Pathogens are inhaled as contaminated droplets.
  • 10. • hematogenous spread (e.g., from tricuspid endocarditis) or by contiguous extension from an infected pleural or mediastinal space. • Once engulfed, the pathogens—even if they are not killed by macrophages—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 exceeded does clinical pneumonia become manifest.
  • 11. • Alveolar macrophages initiate the inflammatory response to bolster lower respiratory tract defenses. • Inflammatory mediators released by macrophages and the newly recruited neutrophils create an alveolar capillary leak. • The capillary leak results in a radiographic infiltrate and rales detectable on auscultation, and hypoxemia results from alveolar filling.
  • 12. PATHOLOGY • Edema • red hepatization • gray hepatization • resolution
  • 13. • Edema- with the presence of a proteinaceous exudate - and often of bacteria—in the alveoli. • This phase is rarely evident in clinical or autopsy specimens because it is so rapidly followed by a red hepatization phase.
  • 14. • red hepatization - presence of erythrocytes in the cellular intraalveolar exudate gives this second stage its name, but neutrophils are also present and are important from the standpoint of host defense. • Bacteria are occasionally seen in cultures of alveolar specimens collected during this phase.
  • 15. • gray hepatization - no new erythrocytes are extravasating, and those already present have been lysed and degraded. • The neutrophil is the predominant cell, fibrin deposition is abundant, and bacteria have disappeared. • This phase corresponds with successful containment of the infection and improvement in gas exchange.
  • 16. • Resolution - the macrophage is the dominant cell type in the alveolar space, and the debris of neutrophils, bacteria, and fibrin has been cleared, as has the inflammatory response.
  • 17. COMMUNITY-ACQUIRED PNEUMONIA • extensive list of potential etiologic agents in CAP includes bacteria, fungi, viruses, and protozoa.
  • 18. • Clinical features – patient is frequently febrile, with a tachycardic response, and may have chills and/or sweats and cough that is either nonproductive or productive of mucoid, purulent, or blood-tinged sputum. • Pleuritic chest pain, gastrointestinal symptoms • increased respiratory rate, use of accessory muscles of respiration.
  • 19.
  • 20. • Palpation may reveal increased or decreased tactile fremitus • percussion note can vary from dull to flat, reflecting underlying consolidated lung and pleural fluid. • Crackles, bronchial breath sounds, and possibly a pleural friction rub may be heard on auscultation.
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  • 27. Management • Oxygen should be administered to all patients with tachypnoea, hypoxaemia, hypotension or acidosis, with the aim of maintaining the PaO2 at or above 8 kPa (60 mmHg) or the SaO2 at or above 92%.
  • 28.
  • 29. • Intravenous fluids – severe illness, older patients and those who are vomiting. Inotropic support may be required in patients with shock.
  • 30.
  • 31. Discharge and follow-up • depends on their home circumstances and the likelihood of complications. • Clinical review should be arranged around 6 weeks later and a chest X-ray obtained if there are persistent symptoms, physical signs or reasons to suspect underlying malignancy.
  • 32. Prevention • Current smokers should be advised to stop. • Influenza and pneumococcal vaccination. • Tackling malnourishment and indoor air pollution, and encouraging immunisation against measles, pertussis and Haemophilus influenzae type b are particularly important in children.
  • 33.