Pneumonia
What is pneumonia?
How do we classify pneumonia?
Classification
How do we classify pneumonia?
Risk Factors for Drug Resistant Pathogens
Pneumonia Mode of transmission
Pneumonia – pathophysiology
Pneumonia - Pathology
Community-acquired pneumonia - Etiology
Community-acquired pneumonia
Community-acquired pneumonia
Special populations
Special populations
Q fever
Clinical manifestations
Signs of bacterial pneumonia
Clinical manifestations
Symptoms
Diagnosis of Community-Acquired Pneumonia
Imaging studies
Diagnosing Pneumonia etiology: is it worth the bother?
Diagnosing Pneumonia: How Much Testing Is Needed?
Sputum
Additional
Treatment – Main questions
British Thoracic Society CAP severity assessment:CURB 65 score
Pneumonia Severity Index (PSI)
Where to Treat Pneumonia: Medical Ward or ICU?
Antibiotic Treatment of Community-Acquired Pneumonia
Initial therapy - Outpatient
Initial therapy – In-patient Non-ICU
Initial therapy - In-patient ICU
Initial therapy - additional
Duration of Therapy
Failure to improve
Complications
CAP - Prevention
VAP
VAP - diagnosis
VAP – diagnosis – quantitive culture
VAP – Treatment
Initial therapy – No MDR risk factors
Initial therapy –MDR risk factors
VAP – Treatment
VAP – Prevention
Lung Abscess
Lung abscess - Etiology
Lung abscess
Lung abscess
Lung abscess - Treatment
Pulmonary infections in immunocompromised patients
HSCT recipients
HSCT recipients - CMV
Solid organ recipients
Human immunodeficiency virus associated pulmonary infections
HIV – respiratory disease
HIV – respiratory disease - PcP
HIV – respiratory disease - PcP
HIV – respiratory disease - TB
HIV – respiratory disease – atypical mycobateria
HIV – respiratory disease - Fungal
Pulmonary infections in cancer
Pulmonary infections in cancer - Aspergillus
6.20M
Категория: МедицинаМедицина

Pneumonia

1. Pneumonia

Y.Gorelik

2. What is pneumonia?

An infectious inflammation of
lung parenchyma, distal
airways and interstitium.

3. How do we classify pneumonia?

4. Classification

Neither radiological or microbiological
criteria are specific for predicting the
cause of pneumonia.
A better approach is to first consider the
clinical circumstances under which
pneumonia acquired
Add the clinical background of the
particular patient

5. How do we classify pneumonia?

Major distinctions (setting of acquisition):
Community Acquired Pneumonia (CAP)
Hospital associated pneumonia (HAP)
Health care associated (HCAP)*
Ventilator-associated pneumonia (VAP)
By anatomy or pathophysiology:
Lobar pneumonia
Bronchopneumonia
Interstitial pneumonia
Aspiration pneumonia
Post-obstructive pneumonia

6. Risk Factors for Drug Resistant Pathogens

Hospitalization of >2 d in previous 90 d
Antibiotics use in previous 90 d
Immunosupression
Non-ambulatory
Tube feeding
Acid suppression
COPD/bronchiectasis
Hemodialysis
CHF

7.

8. Pneumonia Mode of transmission

Bacteria and viruses living in nose, sinuses,
or mouth may spread to lungs
Directly into your lungs (droplets infection)
Aspiration pneumonia
Hematogenous spread (endocarditis. Rarely)
Contigious extension (pleural, mediastinal)

9.

10. Pneumonia – pathophysiology

Alteration of normal oropharyngeal flora.
Depressed Cough and glottis reflexes
(gastric content aspiration)
Impaired mucociliary apparatus
mechanism, alveolar macrophage
dysfunction (overwhelming)
Immune dysfunction

11. Pneumonia - Pathology

Inflammation of lung tissue- edema
Erythrocytes and neutropils in alveolar space – red
hepatization
When neutrophil predominant – grey hepatization
Containment, macrophages predominant -
resulotion
Capillary leak (sputum, even hemoptysis) – imaging
appearance, hypoxemia

12. Community-acquired pneumonia - Etiology

Bacteria - Typical
Atypical Pathogens (Legionella
pneumophila, Chlamydophila pneumoniae,
and Mycoplasma pneumoniae)
Viruses
Fungi
Polymicrobial (10%-15%)

13. Community-acquired pneumonia

Bacteria
S. pneumoniae, Hemophilus influenzae Staphylococcus
aureus, gram negative bacilli
S. pneumoniae was the most common pathogen among
older patients and among those with significant underlying
disease.
Hemophilus infection found in 5%— mostly in patients with
comorbidities.
Staphylococcus aureus - necrotizing pneumonia, abscess
Anaerobs

14. Community-acquired pneumonia

Respiratory viruses (20%-30% in
healthy and patients)
Influenza (A and B)
Human metapneumovirus
Adenovirus
Respiratory syncytial virus
Can precede severe bacterial superimposed
infections

15. Special populations

Alcoholism – S.pneumoniae, anaerobes, K.
pneumoniae, Acinetobacter spp., Mycobacterium
tuberculosis (less common locally)
COPD – H. influenzae, P. aeruginosa, Legionella, S.
pneumoniae, M. catarrhalis, C. pneumoniae
Structural diseases - P. aeruginosa, Burkholderia
cepacia, Staphylococcus aureus
Dementia, stroke – Oral anaerobs, enteric bacteria

16. Special populations

Abscess – Staph aureus, anaerobs, fungi
Ship, hotel, certain establishments – Legionella
Birds (parrots)- chlamidya psittaci
Sheep, goat – Coxiella burnetii
P. aeruginosa – structural lung diseases
Legionella - hematologic malignancy, cancer, severe
renal disease, HIV infection

17. Q fever

18. Clinical manifestations

Abrupt onset
Fever chills
Cough (dry, productive, purulent, mucoid)
Dyspnea (uncorrelated with spread)
GI in 20% of patients
Recent associations to MI

19.

20. Signs of bacterial pneumonia

Hyperthermia (fever, typically >38°C)or hypothermia (<
35°C)
Tachypnea (>18 respirations/min)
Use of accessory respiratory muscles
Tachycardia (>100 bpm) or bradycardia (< 60 bpm)
Central cyanosis
Altered mental status

21. Clinical manifestations

Auscaltation – Crackles, bronchial sounds,
pleural friction rub
Atypical presentation especially in elderly –
general deterioration, confusion, delirium
Most severe presentation – Septic shock

22. Symptoms

Cough, particularly cough productive of sputum, is
the most consistent presenting symptom of bacterial
pneumonia and may suggest a particular
pathogen, as follows
Streptococcus pneumoniae: Rust-colored sputum
Pseudomonas, Haemophilus, and pneumococcal
species: May produce green sputum
Klebsiella species pneumonia: Red currant-jelly
sputum
Anaerobic infections: Often produce foul-smelling
or bad-tasting sputum

23. Diagnosis of Community-Acquired Pneumonia

Diagnosis of CommunityAcquired Pneumonia
Symptoms and signs
Physical exam (sensitivity – 58%,
specificity – 67%)
Laboratory (inflammatory markers)
A new or changed infiltrate on imaging
(sometimes suggestive of etiology)

24. Imaging studies

Chest radiography: The criterion
standard for pneumonia diagnosis
Chest computed tomography scanning
Chest ultrasonography
Radiologists may disagree 10% of the
time in diagnosing pneumonia from
chest films.

25.

26.

27.

28.

29. Diagnosing Pneumonia etiology: is it worth the bother?

30. Diagnosing Pneumonia: How Much Testing Is Needed?

During influenza season, testing for
influenza is indicated for all patients with
pneumonia
Urinary Legionella antigen testing
Pneumococcal urinary antigen
PCR
Serology – IgM rise or seroconversion

31. Sputum

Ensure sample is adequate
Yield of positive cultures is low (~50%)
Interfering factors – patient factors,
treatment
Gram stain can assist in decisions

32.

33.

34. Additional

Blood cultures – positive in 5%-14%
Urine – Legionella serotype 1,
pneumococcal (more prone to FP)
PCR – mostly viral from nasal swabs
Serology – diagnostic, long wait
CRP and PCT help in treatment decisions

35. Treatment – Main questions

Where?
How?

36. British Thoracic Society CAP severity assessment:CURB 65 score

Will help determine where treated (home vs
hospital), and likely mortality.
Any of: confusion, urea> 7mmol/l (42 mg/dL),
respiratory rate>30/min, blood pressure
systolic <90mmHg diastolic<60mmHg, age>65
years
Low (0-1), moderate (2), high (3+) severity
ICU admission indicated by CURB score of 4-5

37. Pneumonia Severity Index (PSI)

Prognosis of mortality - Calculates everity
class and risk of mortality

38. Where to Treat Pneumonia: Medical Ward or ICU?

Any patient with 3 of the following 9 criteria
be considered for ICU
1. Confusion
2. BUN ≥20 mg/dL
3. respiratory rate ≥ 30/min
4. multilobar pneumonia
5. hypoxemia with PaO2/FiO2 < 250
6. platelets < 100,000 mm³
7. hypotension (SBP<90 mm Hg)
8. hypothermia < 36º C
9. white blood cell count < 4,000/mm³.

39. Antibiotic Treatment of Community-Acquired Pneumonia

Antibiotic Treatment of CommunityAcquired Pneumonia
Main challenge – Resistance
Increasing pneumococcal resistance to β-
lactams
Developing resistance to macrolides,
quinolone and tetracyclines
Gram negatives - usually resistant –
quinolones or carbapenems are often used
(pip/taz)

40. Initial therapy - Outpatient

1. Previously healthy and no antibiotics in past 3
months
A macrolide - clarithromycin, azithromycin or
Doxycycline
2. Comorbidities or antibiotics in past 3 months
fluoroquinolone moxifloxacin, levofloxacin or
A β-lactam amoxicillin,amoxicillin/clavulanate;
ceftriaxone, cefuroxime plus a macrolide

41. Initial therapy – In-patient Non-ICU

Fluoroquinolone – moxifloxacin,
levofloxacin
OR
A β-lactam (ceftriaxone, ampicillin,
ertapenem plus a macrolide

42. Initial therapy - In-patient ICU

A β-lactam - ceftriaxone, ampicillinsulbactam,
plus
either azithromycin or a
fluoroquinolone

43. Initial therapy - additional

Pseudomonas
An antipseudomonal β-lactam piperacillin/tazobactam,
cefepime, imipenem, meropenem plus either ciprofloxacin or
levofloxacin
The above β-lactams plus an aminoglycoside amikacin or
tobramycin plus azithromycin
The above β-lactamsf plus an aminoglycoside plus a
fluoroquinolone
MRSA - Add linezolid (600 mg IV q12h) or vancomycin

44. Duration of Therapy

Fevere and markers first to improve. Physical
findings persist longer. X-ray up to 12 weeks
Follow-up x-ray needed!
switched to oral therapy when clinical
improvement, stable and uptaking oral
medicaions
Duration used to be 10-14 days – trials
demonstrated 5 days similar outcomes (even 1
day of ceftriaxone showed substantial results)

45. Failure to improve

Assess after 3 days
Reasons?

46. Complications

Metastatic infection – brain, endocarditis
Abscess, empyema. Complete drainage –
pH < 7
LDH > 1000 U/L
Bacteria on stain or culture
Glucose < 40 mg/dL
loculations

47. CAP - Prevention

Influenza Vaccine
Pneumococcal Vaccine – PCV13
for children elderly (>65) and
immunocompromised

48. VAP

Depends on duration of hospitalization
5-7 days – CAP organisms, MSSA,
enterobacterioceae
Later – MDR, MRSA, pseudomonas, ESBL
On any day 10% of patients will have VAP.
70% among ventilated for 30 days
Clinically similar with other meausres of
assessment for intubated patients

49.

50.

Colonization
Aspiration
MRSA*
VAP
An imbalance between normal host defenses and the ability of
microorganisms to colonize and then invade the lower
respiratory tract.

51. VAP - diagnosis

Difficult due to:
Bacterial colonization
Misinterpretation and DD to infiltrates
Other possible sources of fever,
respiratory impairments
Debate regarding culture approaches

52. VAP – diagnosis – quantitive culture

Certain threshold of burden defines true
infection: 10^6 from endotracheal
aspirate and 10^3 from BAL
False negative BAL – location,
interfering therapy
The approach showed lower antibiotic
use and lower mortality

53. VAP – Treatment

Early therapy is essential
Antibiotic selection pressures leads to infections
with highly resistant bacteria
MRSA
Acinetobacter, stenotrephomonas, burkhoderia
P.aurigenosa intrinsically resistant and develops
further resistance during therapy
Almost no atypical (other than legionella)

54. Initial therapy – No MDR risk factors

Ceftriaxone or cefotaxime or
Moxifloxacin, ciprofloxacin, or
levofloxacin or
Ampicillin/sulbactam or Ertapenem

55. Initial therapy –MDR risk factors

1. A β-lactam: Ceftazidime or Piperacillin/tazobactam
or Imipenem, or meropenem
plus
2. A second agent active against gram-negative:
Gentamicin or tobramycin or amikacin or
Ciprofloxacin or levofloxacin plus
3. An agent active against gram-positive bacterial
pathogens:
Linezolid or Vancomycin

56. VAP – Treatment

Narrow range with culture results
If all cultures negative consider stopping
P.auregenosa and MRSA VAP with high
failure rate (50% and 40% respectively)
Most sensitive clinical parameter to
improvement – oxygenation
High crude mortality (50%-70%)

57. VAP – Prevention

Reduce intubation rates and days
Head elevation

58. Lung Abscess

59. Lung abscess - Etiology

Usually defined as primary (80%) arising
from aspiration and secondary from
anatomic or systemic diseases
Major risk factors in population prone for
aspiration

60. Lung abscess

Aspiration causes pneumonitis and then
necrotizing lesions usually infected with
polymicrobial anaerobs
Secondary infections from anatomic
obstructing lesions more commonly with
gram negatives
Clinically more chronic with anemia and
clubbing in addition to other pneumonia
features

61. Lung abscess

Diagnosis usually made with CT that
established location and type
Procedures like bronchoscopy or
needle aspiration – spillage risk

62. Lung abscess - Treatment

Primary – gram positive and anaerobs coverage –
clindamycin or amoxicillin/clavulanate
Secondary – by organism
Around 7 days for response
Long duration of therapy
10%-20% do not respond especially in large lesions
2% mortality in primary and around 75% in
secondary

63. Pulmonary infections in immunocompromised patients

64. HSCT recipients

Complete immunodeficiency
immediately after transplant
First days granulocytopenic
Bacterial infections – organisms from
patient, nosocomial
Fungal infections – Aspergillus, candida,
reactivation – histoplasmosis
P.jivorecii (PcP)
Parasitic – Toxoplasma
Viruses – HSV-1 (exclusive to HSCT), CMV

65.

Early 1st
month
1-4 months
Late > 6
months
• Aerobic bacteria
• Candida
• Aspergillus
• HSV
• CMV
• Seasonal viruses
• P.Jivorecii
• Pneumococci
• P.Jovorecii
• Nocardia

66. HSCT recipients - CMV

Classic onset – 30-90 days post
Highest risk when recipient is seropositive
and the donor is seronegative (opposite in
solid organ)
Ganciclovir prophylaxis prevents disease
but has high risk – preemptive rather than
prophylactic approach used
CMV pneumonia highly fatal
Treatment with ganciclovir/foscarnet with
IVIg used

67.

68. Solid organ recipients

immunosuppressed for longer periods (often
permanently)
Pulmonary infections similar to hsct transplant
recipients. Fungal infections occur later
CMV is permanent risk due to
immunosuppression
Nocardia – gram positive bacilli. Mostly in the
middle period after transplant
Localized pulmonary disease often with
cavitary lesions
Prophylaxis with TMP-SMX (used mostly for
p.jivorecii and toxoplasma)

69.

Early 1st
month
1-4 months
Late > 6
months
• Aspiration pneumonia
• VAP - bacterial
• CMV (highest risk in lung)
• Aspergillus (highest in lung)
• P.Jivorecii
• P.Jovorecii
• Nocardia
• Activeted granulomatous disease
• TB

70.

71. Human immunodeficiency virus associated pulmonary infections

72. HIV – respiratory disease

Recurrent pneumonia, tuberculosis and
p.jivorecii pneumonia among most
common AIDS defining illnesses
Pneumococcal - most common bacterial
pneumonia. 100-fold increase in rate of
bacteremia
Immunization recommended. Most
effective when CD4+ > 200

73. HIV – respiratory disease - PcP

Single most common cause of pneumonia
50% unaware of HIV
In 79% cd4+ < 100/ μL
Incidence near zero in cART + TMP-SMX
receiving patients
Symptoms – fever, dry cough, pleuritic
pain, indolent course
Extrapulmonary often seen (ophthalmic,
vasculitis, hematologic, renal)

74. HIV – respiratory disease - PcP

Most common finding on x-ray – normal
(no perihilar infiltrates)
Laboratory of little value – elevated LDH,
increased A-a gradient
Diagnosis requires culture or PCR from BAL
Treatment – TMP-SMX (3 wks) – high rate of
adverse effects in HIV patients
Glucocorticoids if PaO2 < 70 or A-a > 35
Prophylaxis – in previously infected, CD4+
<200/15%, fever > 2 wks, candidiasis

75. HIV – respiratory disease - TB

Worldwide 33% of HIV associated death
Develops early in the course of HIV
(median CD4+ of 330)
Clinical mostly typical pattern – fever,
night sweats, dyspnea, cavitary lesions in
upper lobes
Treatment involves risk of IRIS – should
apply preventive protocols (if cd4+ level
allows)
PPD > 5 mm, IGRA+ or close households –
considered latent – 9 m dual therapy

76. HIV – respiratory disease – atypical mycobateria

Mostly MAC – usually from
environment
Late complication
presenting as disseminated
(85% bacteremic)
Systemic presentation
common
Abnormal x-ray only in 25%
Macrolide therapy
Rhodococcus equi –
pulmonary cavitary
disease (mogth resemble
TB), extrapulmonary lesions
and bacteremia

77. HIV – respiratory disease - Fungal

HIV – respiratory disease Fungal
Cryptococcal – fever, cough,
hemoptysis, abnormal x-ray (varying
pattern) and CNS involvement in
>90%
Aspergillus – not a common HIV
agent
Histoplasmossis – mostly as
dissemination

78. Pulmonary infections in cancer

Local factors – tumor, inflammation,
obstruction, radiation
Systemic factors – metastatic
disease, chemotherapy
Differential diagnosis

79. Pulmonary infections in cancer - Aspergillus

Can colonize skin and airways
Invades lungs (IPA)
Diagnosis requires triad of host,
microbiologic and imaging evidence
Cough, pleuritic pain, hemoptysis
Culture, galactomannan (blood,
sputum)
Imaging – infiltrates, halo sign,
crescent

80.

81.

Thank You
English     Русский Правила