A presentation during our Medicine Posting (Internship days)

1. A Discussion On The Killer Infectious Disease Of
Lungs:
Pneumonia
Presented By:
Dr. Pravin Prasad
Dr. Rabin Babu Paudyal
Interns, Medicine Unit III

2. PNEUMONIA: INTRODUCTION
• Pneumonia is an infection of the pulmonary parenchyma.
(Harrison- 18th Ed)
• Pneumonia is defined as an acute respiratory illness
associated with recently developed radiological pulmonary
shadowing which may be segmental, lobar or multilobar.
(Davidson- 21st Ed)
• Pneumonia was typically classified as community-acquired
(CAP), hospital-acquired (HAP), or ventilator-associated
(VAP).
• Over the past two decades, however, some persons
presenting as outpatients with onset of pneumonia have
been found to be infected with the multidrug-resistant (MDR)
pathogens previously associated with HAP: - thus
development of the term Health Care–associated
Pneumonia (HCAP).

3. Pneumonia: Classification I
A. Classification By Site
Lobar Pneumonia
Bronchopneumonia
Interstitial Pneumonia

4. Pneumonia: Classification II
B. Classification By Aetiology
• Primary Pneumonia
• Secondary Pneumonia (including Aspiration
Pneumonia)
• Suppurative Pneumonia (necrotizing pneumonia)
Common Organisms Less Common Organisms
Streptococcous pneumoniae Klebsiella pneumoniae
Haemophilus influenza Streptococcus pneumonia
Moraxella catarrhalis Pseudomonas aeruginosa
Staphylococcus aureus Coxiella burnetii
Legionella pneumophilia Chlamydia pneumoniae
Mycoplasma pneumoniae Chlamydia psittaci
Actinomyces israeli Viruses (including SARS)
Table 1: Organisms responsible for primary pneumonia

5. Pneumonia: Classification III
C. Classification by mode of acquiring pneumonia
• Community-acquired Pneumonia
• Hospital acquired pneumonia, or Ventilator associated
pneumonia)
• Health Care Associated Pneumonia
• Pneumonia in immuno-compromised host

6. Pneumonia: Pathophysiology
• 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.
• Aspiration from the oropharynx; (most
common)
• Inhalation of contaminated droplets;
• Hematogenous spread
• Contiguous extension.

7. Pneumonia: Pathophysiology
(contd.)
• Defense Mechanisms against Pneumonia
• Hairs and turbinates of the nares
• Branching architecture of the
tracheobronchial tree
• Muco-ciliary clearance and local
antibacterial factors
• Gag reflex and the cough mechanism
• the normal flora adhering to mucosal
cells of the oropharynx
• Alveolar Macrophages, local proteins
(e.g., surfactant proteins A and D)

8. Pneumonia: Pathophysiology (contd.)
• Only when the capacity of the alveolar macrophages to
ingest or kill the microorganisms is exceeded does clinical
pneumonia become manifest.
• The alveolar macrophages initiate the inflammatory response
to bolster lower respiratory tract defenses.
Mediators Responsible Effects
IL-1 and TNF Fever
IL – 8 , GCSF stimulates
release & attraction of
neutrophils to the lungs
Causes peripheral leucocytosis,
increased purulent secretions
Inflammatory mediators
(macrophages) & neutrophils
Localised alveolar capillary leak
Table 2: Mediators responsible in patho-physiology of Pneumonia

9. Pneumonia: Pathophysiology (contd.)
Mechanism Clinical Features
Leaky alveolar capillaries
Hemoptysis
Radiologic infiltrates
Rales on auscultation
Alveolar filling and action of bacterial
pathogens
Hypoxemia
Decreased compliance of lungs Dyspnoea
Reduction in lung volume and
compliance
Intra-pulmonary shunting of blood
Death

10. Stages/Phases of Pneumonia Characteristic Features
Oedematous Phase  Alveoli filled with proteinaceous
exudate and bacteria
 Rapidly followed by Red hepatization
phase
Stage of Red hepatization  Presence of erythrocytes in the
cellular intraalveolar exudate
 Neutrophil influx
 Bacteria can be seen in specimens
Stage of Gray hepatization
(successful containment of the infection
& improvement in gas exchange)
 Erythrocytes extravasation ceases,
extravasated ones get lysed and
degraded
 Neutrophils predominant
 Abundant fibrin deposition
 Disappearance of bacteria
Stage of Resolution  Macrophages reappear
 Debris (PMN, Bacteria, fibrin) cleared
 Inflammatory response cleared
Pneumonia: Pathology
Table 3: Different Pathologic Phases of Pneumonia
*Has been described best for lobar pneumococcal pneumonia.

11. CAP & HAP: A Comparison
Community Acquired Hospital Acquired
Definition It indicates pneumonia occuring in
a person in a community (outside
hospital)
Refers to a new episode of
pneumonia occurring at least 2
days after admission to hospital.
Predisposing
Factors
Cigarette smoking
Upper respiratory tract infections
Alcohol
Corticosteroid therapy
Old age
Recent influenza infection
Indoor air pollution
Reduced host defences against
bacteria
Aspiration of
nasopharyngeal/gastric
secretions
Bacteria introduced into lower
respiratory tract
Bacteraemia
Mode of
Spread
Droplet Infection
Infecting
Agent
S. Pneumoniae, S. aureus, H.
influenza
Viruses (influenza, parainfluenza,
measles, Herpes simplex, Varicella,
CMV)
Early-Onset: similar to CAP
Late-Onset: Escherichia,
Pseudomonas, Klebsiella,
MRSA, anaerobes

12. CAP & HAP: Presentation(contd.)
Community Acquired Hospital Acquired
 Can vary from indolent to fulminating
presentation
 Pulmonary Symptoms : breathlessness,
cough,-non-productive or productive
(mucoid, purulent , blood stained)
haemoptysis, plueritic chest pain, may able
to speak sentences/ short of breath
 Systemic Features : fever a/w chills n
rigors, tachycardia, vomiting, decreased
appetite, headache, fatigue, myalgias,
arthralgia
 Elderly: New-onset/ progressive confusion
 Severely ill: septic shock or organ-failure
 Tachypnoea, use of accessory muscles,
increased/decreased vocal fremitus,
 Percussion note: dull to flat
 Bronchial Breathing, Crackles
 Whispering pectoriloquy, pleural friction rub
 Universally agreed diagnostic
criteria lacking
 Should be considered in any
hospitalised /ventilated patient
who develops:
 purulent sputum (or
endotracheal secretions),
 new radiological infiltrates,
 an otherwise unexplained
increase in oxygen
requirement,
 a core temperature > 38.3°C,
and
 leucocytosis or leucopenia.

13. CAP & HAP: Investigation
Community Acquired Hospital Acquired
Chest Radiology: to confirm the
diagnosis and to exclude complications
Pulse oximetry to monitor response to
oxygen therapy, if SaO2 < 93%, features
of severe pneumonia, identify ventilatory
failure or acidosis
Cell count: neutrophil leucocytosis
Microbiologic Studies: for severe CAP
and for those that do not respond to initial
therapy (Gram stain, sputum culture,
blood culture, Polymerase Chain
Reaction, Serology, Antigen Detection)
Renal Function Tests: Urea &
electrolytes
Liver Function Tests
Elevated C-Reactive Protein
Circulating biomarkers may assist
with the diagnosis but are currently
non-specific.
Appropriate investigations are similar
to CAP, microbiological confirmation
preferrable.
In mechanically ventilated patients,
bronchoscopy-directed protected
brush specimens or bronchoalveolar
lavage (BAL) may be performed.
Endotracheal aspirates are easy to
obtain but less reliable.

14. Chest Radiology In Pneumonia
Left Lobar Pneumonia
with pleural effusion
Right Middle Lobar
Pneumonia
Right Upper Lobar
Pneumonia
Right Upper Lobe Pneumonia
with air bronchograms

15. Hospital Care Associated Pneumonia
• HCAP represents a transition between classic CAP and typical HAP
• Refers to the development of pneumonia in a person who has spent at
least 2 days in hospital within the last 90 days, attended a
haemodialysis unit, received intravenous antibiotics, or been resident in
a nursing home or other long-term care facility. (Davidson-21st Ed.)
• MRSA in particular is more common in HCAP than in traditional
HAP/VAP.
• Patients at greatest risk for HCAP are not well defined.
• Patients from nursing homes are not always at elevated risk for
infection with MDR pathogens.
• Low risk of MDR infection if they have not recently received
antibiotics and are independent in most activities of daily living.
• Patients receiving home infusion therapy or undergoing chronic
dialysis are probably at particular risk for MRSA pneumonia
• In general, management of HCAP due to MDR pathogens is similar to
that of MDR HAP/VAP.

16. Pneumonia: Severity Assessment
• There are currently two sets of criteria:
• Pneumonia Severity Index (PSI), a prognostic model
used to identify patients at low risk of dying; and
• CURB-65 criteria, a severity-of-illness score.
Assessment for need for ICU
care provided by severity
criteria proposed by the
Infectious Diseases Society
of America (IDSA) and the
American Thoracic Society
(ATS)
≥
≥
≤ ≤
≥

17. CAP TREATMENT:
GENERAL CONSIDERATION
• Adequate hydration, oxygen therapy for hypoxemia, and assisted
ventilation
• Patients with severe CAP who remain hypotensive despite fluid
resuscitation may have adrenal insufficiency and may respond to
glucocorticoid treatment.
• Immunomodulatory therapy in the form of drotrecogin alfa (activated)
should be considered for CAP patients with persistent septic shock
and APACHE II scores of 25, particularly if the infection is caused by
S. pneumoniae.
• Once the etiologic agent(s) and susceptibilities are known, therapy
may be altered to target the specific pathogen(s).
• Switch to oral treatment is appropriate as long as the patient can
ingest and absorb the drugs, is hemodynamically stable, and is
showing clinical improvement.
• The duration of treatment for CAP has generated considerable
interest

18. CAP: Empirical Treatment for
Out-Patients
Modality Regimen
Previously healthy
and no antibiotics in
past 3 months:
A macrolide [clarithromycin (500 mg PO bid) or azithromycin
(500 mg PO once, then 250 mg qd)] or
Doxycycline (100 mg PO bid)
Comorbidities or
antibiotics in past 3
months: select an
alternative from a
different class
A respiratory fluoroquinolone [moxifloxacin (400 mg PO
qd), gemifloxacin (320 mg PO qd), levofloxacin (750 mg PO
qd)] or
A β-lactam [preferred: high-dose amoxicillin (1 g tid) or
amoxicillin/clavulanate (2 g bid); alternatives: ceftriaxone (1–
2 g IV qd), cefpodoxime (200 mg PO bid), cefuroxime (500
mg PO bid)] plus a macrolide
In regions with a high rate of "high-level" pneumococcal macrolide resistance,
consider alternatives listed above for patients with comorbidities.

19. CAP: Empirical Treatment for
In-Patients
Modality Regimen
Non ICU Patients  A respiratory fluoroquinolone [moxifloxacin (400 mg PO or IV
qd), gemifloxacin (320 mg PO qd), levofloxacin (750 mg PO or
IV qd)]
 A β-lactam [cefotaxime (1–2 g IV q8h), ceftriaxone (1–2 g IV
qd), ampicillin (1–2 g IV q4–6h), ertapenem (1 g IV qd in
selected patients)] plus a macrolide [oral clarithromycin or
azithromycin or IV azithromycin (1 g once, then 500 mg qd)]
ICU Patients  A β-lactam [cefotaxime (1–2 g IV q8h), ceftriaxone (2 g IV qd),
ampicillin-sulbactam (2 g IV q8h)] plus
 Azithromycin or a fluoroquinolone

20. CAP: Empirical Treatment
Special Concerns
Organism being
considered
Treatment Regimen
Pseudomonas  An antipneumococcal, antipseudomonal β-lactam
[piperacillin/tazobactam (4.5 g IV q6h), cefepime (1–2
g IV q12h), imipenem (500 mg IV q6h), meropenem
(1 g IV q8h)] plus either ciprofloxacin (400 mg IV
q12h) or levofloxacin (750 mg IV qd)
 The above β-lactams plus an aminoglycoside
[amikacin (15 mg/kg qd) or tobramycin (1.7 mg/kg
qd) and azithromycin]
 The above β–lactams plus an aminoglycoside
plus an antipneumococcal fluoroquinolone
CA-MRSA  Add linezolid (600 mg IV q12h) or vancomycin (1 g IV
q12h).

21. CAP TREATMENT:
FAILURE TO RESPOND
• Patients who are slow to respond to therapy should be
reevaluated at about day 3 (sooner if their condition is
worsening rather than simply not improving)
• Check the drug, dose of the correct drug
• Pathogen resistant to the drug selected, or a sequestered
focus (e.g., a lung abscess or empyema).
• Consider possibility of an unsuspected pathogen (e.g., CA-
MRSA, M. tuberculosis, or a fungus).
• Re-consider your Diagnosis: tuberculosis, pulmonary edema,
pulmonary embolism, lung carcinoma, radiation and
hypersensitivity pneumonitis, and connective tissue disease
involving the lungs.
• Nosocomial superinfections—both pulmonary and
extrapulmonary

22. HAP: Emperical Treatment
Categories Treatment
Patients without
Risk Factors for
MDR Pathogens
 Ceftriaxone (2 g IV q24h) or
 Moxifloxacin (400 mg IV q24h), ciprofloxacin (400 mg IV
q8h), or levofloxacin (750 mg IV q24h) or
 Ampicillin/sulbactam (3 g IV q6h) or
 Ertapenem (1 g IV q24h)
Patients with Risk
Factors for MDR
Pathogens
1. A β-lactam:
Ceftazidime (2 g IV q8h) or cefepime (2 g IV q8–12h) or
Piperacillin/tazobactam (4.5 g IV q6h), imipenem (500 mg
IV q6h or 1 g IV q8h), or meropenem (1 g IV q8h) plus
2. A second agent active against gram-negative bacterial
pathogens:
Gentamicin or tobramycin (7 mg/kg IV q24h) or amikacin
(20 mg/kg IV q24h) or
Ciprofloxacin (400 mg IV q8h) or levofloxacin (750 mg IV
q24h) plus
3. An agent active against gram-positive bacterial pathogens:
Linezolid (600 mg IV q12h) or
Vancomycin (15 mg/kg, up to 1 g IV, q12h)

23. PNEUMONIA: COMPLICATIONS
• Para-pneumonic effusion
• Empyema
• Retention of sputum causing lobar collapse
• Pulmonary embolism and DVT
• Pneumothorax (S. aureus)
• Suppurative pneumonia/ lung abscess
• ARDS, renal failure, multi-organ failure
• Ectopic abscess formation (S. aureus), Metastatic infection
• Pericarditis, hepatitits, myocarditis, meningoencephalitis
• Pyrexia due to drug hypersensitivity
• Exacerbation of comorbid illnesses.
• Complicated pleural effusion: diagnostic/therapeutic tapping required
• If the fluid has a pH of <7, a glucose level of <2.2 mmol/L, and a lactate
dehydrogenase concentration of >1000 U/L or if bacteria are seen or
cultured, then the fluid should be drained; a chest tube is usually required.

24. PNEUMONIA: FOLLOW UP
• Fever and leukocytosis usually resolve within 2–4 days in
otherwise healthy patients with CAP, but physical findings
may persist longer.
• Chest radiographic abnormalities are slowest to resolve and
may require 4–12 weeks to clear
• Patients may be discharged from the hospital once their
clinical conditions are stable, with no active medical
problems requiring hospital care.
• For a patient whose condition is improving and who (if
hospitalized) has been discharged, a follow-up radiograph
can be done ~4–6 weeks later.
• If relapse or recurrence is documented, particularly in the
same lung segment, the possibility of an underlying
neoplasm must be considered.

25. PNEUMONIA: PROGNOSIS
• Depends on
• Patient's age,
• Comorbidities, and
• Site of treatment (inpatient or outpatient).
• Young patients without comorbidity do well and usually
recover fully after ~2 weeks.
• Older patients and those with comorbid conditions can take
several weeks longer to recover fully.
• Overall mortality rate for the outpatient group is <1%.
• Overall mortality rate for Inpatient group is estimated at 10%,
with ~50% of deaths directly attributable to pneumonia.

26. PNEUMONIA: PREVENTION
• The main preventive measure is vaccination.
• In the event of an influenza outbreak, unprotected patients at
risk from complications should be vaccinated immediately
and given chemoprophylaxis with either oseltamivir or
zanamivir for 2 weeks—i.e., until vaccine-induced antibody
levels are sufficiently high.
• Because of an increased risk of pneumococcal infection,
even among patients without obstructive lung disease,
smokers should be strongly encouraged to stop smoking.
• 7-valent pneumococcal conjugate vaccine: produces T cell–
dependent antigens that result in long-term immunologic
memory.

27. From our Department….
• Sama Prasad, 55 years Male, non smoker, non alcohol
consumer, resident of Bara, working as labour in cement
factory for 15 yrs, married, Hindu, came to ED 6 days back
with:
• Cough-productive, scanty, yellowish for 3 days
• Fever- a/w chills & rigors, not documented for 2 days
• Loss of appetite for 2 days
• No significant past medical, surgical, personal, family history

28. From our Department….
• General Examination:
• Ill looking, conscious, oriented to time, place & person
• No signs of pallor, icterus, cyanosis, clubbing, koilonychiya,
lymphadenopathy, edema, dehydration
• Febrile (100
o
F), tachypnoeic (30 breaths/min), pulse 100 b/miin,
BP 110/60 mm of Hg
• Chest Examination:
• Inspection- B/L symmetrical & elliptical, use of accessory muscle
present
• Palpation- no mediastinal shift, increased vocal fremitus over
right infra-mammary region, reduced chest expansion on right
side
• Percussion- dull note over same area
• Auscultation- decreased air entry & coarse crepitations over
same area, wheeze over right subscapular area as well
• Other Systems Examination: No Significant Findings

29. From our Department….
• Provisional Diagnosis: Right Middle Zone Pneumonia
• Investigations requested:
• Hb% - 10.25%
• TLC – 24,700, neutrophilic predominance
• RBC & Platelet count – Within normal limit
• Chest X-ray, Postero-Anterior View
CURB-65 Score: 2/5; Hospital Supervised Treatment (Short stay
Inpatient )

30. From our Department….
• Pt. treated on Non-ICU Inpatient basis.
• Coverage for Pseudomonas & CA-MRSA considered
• Emperical Treatment Started with:
• Tab. Levoflox 500 mg PO OD
• Inj. Durataz (Tazobactam & Piperacillin) 4.5gm IV TDS
(Pseudomonas coverage)
• Tab. Linez (Linezolid) 600 mg PO BD (CA-MRSA
coverage)
• Supportive Treatment:
• Tab. Nacfil 600 mg PO BD
• Syp. Bronchosolvin 10 PO TDS
• Tab. Pantium 40mg PO OD
• O2 inhalation if SpO2 < 90%
• Nebulization with I:NS 6 hourly

31. REFERENCES
• Douglas, G; Nicol, F; Robertson, C; Macleod’s Clinical
Examination, 12th Ed. 2009
• Davidson’s Principles and Practice of Medicine, 21st Ed. 2010
• Mathew, K. G. Aggarwal, P. Medicine Prep Manual for
Undergraduates, 3rd Ed. 2010
• Harrison’s Principle of Internal Medicine- 18th Ed. 2012
• http://laboratorysciencereview.tumblr.com/post/61505647877
• http://emedicine.medscape.com/article/360090-overview#a19