Good Morning!

2015 Schedule

October 12 Approach to Patient with

Disease of the Respiratory System
October 13 Pneumonia- Community-acquired
October 15 Pneumonia- CAP-LTCFs, Aspiration,
Healthcare-associated
October 16 ARDS
October 17 EXAMINATION
Approach to the patient
with disease of the
respiratory system
Vinci L. Urgel, M.D.
History & physical examination are the
cornerstones for establishing diagnosis!
History
 Occupational & personal history
Exposure to hazards
asbestos coal air conditioners
beryllium silica furnace humidifiers
Work history
duties duration of exposure
protective devices illness in fellow workers
Contact with animals
Residence & travel history
Alcohol intake/ substance abuse
Sexual history
Smoking history: pack-years
Drug exposure

Drug Possible Effect

b-adrenergic blockers Bronchospasm
NSAID
Oral contraceptives Pulmonary embolism
Hydralazine SLE
Procainamide
Aminoglycosides Respiratory muscle
weakness
Bleomycin Interstitial infiltrative
Nitrofurantoin diseases
Cyclophosphamide
Methotrexate
ASA Noncardiogenic pulmo
edema
 Family history

Asthma
Pulmonary emphysema
Cystic fibrosis
Kartageners syndrome
Infections- TB, fungal infections,
schistosomiasis
 History
Dyspnea
respiratory vs. cardiovascular etiology
Chest pain
inflammation of pleura
pneumonia, pulmo embolism, TB, malignancy
pleuritic pain
local discomfort- diseases involving mediastinal organs
referred pain- intercostal neuritis (Herpes zoster)
myositis
costochondral disturbances
myocardial ischemia
pericarditis
esophageal disease
aortic dissection & aneurysm
 History
Cough & expectoration
productive- inflammatory process
non-productive- irritative process
chronic- chronic bronchitis, smokers cough,
TB, lung neoplasms
acute- viral & bacterial infections

Character & quantity of expectorated material

bronchiectasis, lung abscess, necrotizing pneumonia-
purulent sputum w/c may be foul- smelling, blood- streaked
pulmonary edema- pink, frothy, watery
acute & chronic bronchitis- mucoid or mucopurulent
pneumonia- bloody or rusty
paroxysms of cough- asthma
 History
Hemoptysis
faint streaking of sputum with blood- acute
infections, pulmonary thromboembolism, TB,
critical mitral stenosis, lung neoplasms,
bronchiectasis
frankly bloody- pulmonary thromboembolism
with pus- pneumonia, bronchiectasis, lung abscess
dilute, pink, frothy- acute pulmonary edema

inflammatory or infectious airways diseases

localized or diffuse parenchymal diseases
vascular diseases: PTE, pulmo AV malformation
Nasopharyngeal, esophageal, or gastric sources?
Physical Examination
General principles of P. E.

Inspection
Palpation
Percussion
Auscultation
Inspection
Rate & pattern of breathing
Depth & symmetry of lung expansion

Palpation
Symmetry of lung expansion
Symmetry of tactile fremitus
Focal tenderness

Percussion
Relative resonance or dullness
Auscultation
Quality & intensity of BS
Presence of extra or adventitious sounds

Vesicular BS (inspiration time > expiration time)-

normal at periphery of lungs
Diminished BS or absent- endobronchial
obstruction, air/ liquid in pleural space
Bronchial BS- consolidation
Listen to spoken/ whispered words:
Bronchophony- egophony (E becomes more like A)
Whispered pectoriloquy
Auscultation
Adventitious sounds
Crackles
discontinuous, inspiratory sounds
opening & closing of alveoli & small airways
Wheezes
high- pitched sounds more prominent during expiration
oscillation of airway walls when there is airflow limitation
Rhonchi
low- pitched vibratory sound
interaction bet. fluid in airway lumen & moving air
Pleural friction rub
gritty sound
inflamed pleural surfaces rub against each other
Stridor
during inspiration
airflow through narrowed upper airway
 Typical chest Examination Findings
Condition Percus- Fremitus Breath Voice Adventitious
sion Sounds Transmission Sounds

Normal Resonant Normal Vesicular Normal Absent

(at
bases)
Consolidation Dull Bronchial Bronchophony, Crackles
/atelectasis whispered
(patent AW) pectoriloquy,
egophony

Consolidation Dull Absent

/atelectasis
(blocked AW)
 Typical chest Examination Findings

Condition Percus-sion Fremitus Breath Voice Adventiti

Sounds Trans- sounds
mission
Asthma Resonant Normal Vesicular Normal Wheezing

Interstitial Resonant Normal Vesicular Normal Crackles

Lung Disease
Emphysema Hyper-resonant Absent or
wheezing
Pneumo- Hyper-resonant Absent
thorax
Pleural Dull Absent or
effusion pleural fric
rub
General P. E.
lymph nodes in cervical & supraclavicular
regions
mentation/ level of sensorium
teeth & gums
clubbing of digits
systemic diseases with pulmonary
complications- SLE, scleroderma, RA
respiratory diseases with PE findings not
related to respiratory system- ex.
sarcoidosis
uveitis, erythema nodosum, skin granuloma
Diagnostic tests
Chest radiography
often the initial diagnostic study
performed to evaluate patients with
respiratory symptoms
past CXR films important for comparison
usual views:
PA/ AP
lateral upright
lateral decubitus
Chest PA
Lateral Upright
Lateral Decubitus
Lordotic
Chest radiography

radiographic pattern:
localized region of opacification involving lung
parenchyma
nodule- < 3 cm diameter
mass- > 3 cm diameter
infiltrate
diffuse disease with increased opacification:
alveolar
interstitial
nodular
increased radiolucency
localized- cyst or bulla
generalized- emphysema
Chest radiography

detection of pleural disease

air/ fluid in pleural space

abnormal appearance of hila &/or

mediastinum- mass or LN enlargement
Additional diagnostic evaluation

Computed tomographic scanning of chest

more sensitive than CXR
suggest specific diagnosis based on pattern of abnormality
Pulmonary function tests
ABG
Oximetry
Bronchoscopy
Examination of sputum, pleural fluid, bronchial
washing
Skin tests
Scratch or intradermal tests
Environmental Lung
Diseases
Vinci L. Urgel, M.D.
 Occupational Lung Diseases

History & Physical Examination

Pulmonary Function Tests, Chest
Radiography, & Other Diagnostic
Tests
Measurement of Exposure
 History & Physical Examination
specific contaminants
personal respiratory protection devices
site & ventilation of work spaces
similar complaints from coworkers
temporal association of exposure at work & Sx
alternative sources for potentially toxic exposures-
hobbies, home
short-term exposures to potential toxic agents in
distant past
P.E.
determine nature & severity of pulmonary condition
non-specific findings
 Pulmonary Function Tests
1) Spirometry
Obstructive pattern
reduced FEV1/FVC < 70%
usually caused by organic dusts, chemical agents
seen in asthma, COPD
Restrictive pattern
reduced FEV1
reduced FVC
usually caused by mineral dusts
2) Diffusing Capacity
3) Lung Volumes
Spirometry

FVC

FEV1/FVC > 0.70

Normal
 Spirometry

FEV1/FVC < 0.70

Obstructive pattern
 Spirometry

FEV1/FVC > 0.70

Restrictive pattern
 Chest Radiograph
Detect & monitor pulmonary response to
mineral dusts
International Labour Organisation (ILO)
International Classification of Radiographs
of Pneumoconioses
wnature & size of opacities
wextent of parenchymal involvement
wlacks specificity
wmay over- or underestimate the
functional impact of pneumoconiosis
 Computed Tomography
Conventional
High resolution

~ improve sensitivity of identifying diffuse

parenchymal abnormalities
~ earlier detection of silicosis & asbestosis
 Other Diagnostic Procedures
Evaluation of heavy metal
concentrations in urine- arsenic,
cadmium
Bacteriologic studies- TB, anthrax
Fungal studies- coccidioidomycosis,
histoplasmosis
Serologic studies- psittacosis, Q fever
Lung biopsy
 Measurement of Exposure
Environmental sampling
Individual exposure to specific agents
Important factors:
solubility
particle size
chemical composition
mechanical properties
immunogenecity/ infectivity
 Occupational Lung Diseases
Diseases caused by various agents
Inorganic dusts
~asbestos, silica, coal, beryllium, etc.
Organic dusts
~cotton, grain dust, moldy hay
Toxic chemicals
Environmental respiratory carcinogens
Occupational asthma
Lung diseases caused by
inorganic dusts
 Asbestosis
Asbestos
generic term for several different
mineral silicates:
chrysolite anthophyllite
amosite crocidolite
exceptional thermal & electric
insulation properties
presently, mostly replaced with
synthetic mineral fibers
 Asbestosis

Occupational exposures:
mining, milling, manufacture of asbestos
products
building trade (i.e. pipe fitters,
boilermakers, demolition workers)
 Asbestosis
diffuse interstitial fibrosing disease of lung
directly related to intensity & duration of
exposure (moderate- severe exposure x >10 yrs)
in immediate or distant past
PFT: restrictive pattern, reduced flow rate,
decreased diffusing capacity
phagocytes react with transition metals on fiber
surface reactive O2 species
proinflammatory effects fibrotic lesions
 Asbestosis
Diagnosis
Chest X-Ray
Pleural plaques
~ thickening/ calcification along parietal pleura
(lower LFs, diaphragm, cardiac border)
~ indicates past exposure
Pleural effusion
~ sterile, serous or blood-stained exudate
~ may be bilateral
~ may be slowly progressive or may resolve
spontaneously
Irregular or linear opacities first noted in lower
LFs, spreading into middle & upper LFs
~ indistinct heart border
~ ground glass appearance
 Asbestosis

Diagnosis

High-resolution CT Scan
subpleural curvilinear lines 5- 10 cm in
length parallel to pleural surface
 Asbestosis
Lung cancer
most frequent cancer associated with asbestos
exposure
squamous cell carcinoma or adenocarcinoma
develops 15- 19 years after first exposure
the greater the exposure to asbestos, the greater
the risk of lung cancer
smoking multiplies the risk of lung cancer in
persons who are exposed to asbestos
surveillance studies
sputum cytology
chest x-ray
HRCT
 Asbestosis
Mesothelioma
o pleural & peritoneal
o associated with asbestos exposure (even < 1- 2
years, 20- 25 years in past)
o peak incidence: 30- 35 years after initial asbestos
exposure
o dont appear to be associated with smoking
o generally locally invasive but 50% metastasize
o death usually results from local extension
o most present with pleural effusion (w/o shift of
mediastinum)
o Dx: needle biopsy or open lung biopsy
 Silicosis
exposure to free silica (SiO2) or
crystalline quartz
occupational exposures:
mining
stone cutting (i.e. clay, glass, cement)
foundry work packing of silica flour
quarrying of granite
abrasive industries
 Silicosis
Acute silicosis
sandblasting in confined spaces,
tunneling through rock with high
quartz content, manufacture of
abrasive soaps
~10 months exposure
may be rapidly fatal < 2 years
CXR: profuse miliary infiltration or
consolidation
 Silicosis
Long-term, less intense exposure
15- 20 years

CXR:
small rounded opacities in upper lobes
hilar adenopathy

eggshell pattern- calcification of hilar

nodes
reticular pattern of irregular densities in
upper LFs
 Silicosis
Progressive Massive Fibrosis (PMF)
progressive nodular fibrosis with coalescence &
formation of nonsegmental conglomerates of
irregular masses > 1 cm in diameter which become
quite large
PFT: restrictive & obstructive ventilatory pattern
ventilatory failure in late stages
CT scan:
identify nodules at posterior aspect of upper lobes
better than CXR in assessing size & extent of lesions
Silicosis increase risk of acquiring M. tuberculosis
& atypical mycobacterial infections
Silicosis & (+) tuberculin test ---> treat for TB
 Silicosis
Other less hazardous silicates:
Fullers earth diatomaceous earths
kaolin mica
silica gel carbonate dusts
soapstone cement dusts
Talc dust
~ may be contaminated with asbestos &/or free
silica
~ acute talcosis: cough, cyanosis, labored
breathing
~ severe progressive fibrosis with respiratory
failure
~ associated with fibrosis &/or pleural or lung
cancer
 Coal Workers Pneumoconiosis
Exposure to coal dust
Simple CWP
12% of all miners
in 50% of anthracite miners (less in bituminous
miners)
> 20 years work on coal face
Sx similar & additive to effects of smoking on
devt of chronic bronchitis & obstructive lung
disease
CXR
~ early- small, irregular opacities (reticular
pattern)
~ prolonged exposure- small, rounded, regular
opacities (nodular pattern)
 Coal Workers Pneumoconiosis
Complicated CWP
CXR:
~ nodules from 1 cm in diameter to size
of entire lobe (in upper half of lungs)
~ a form of PMF
~ decreased diffusing capacity
~ may result to premature mortality
 Coal Workers Pneumoconiosis

Caplans Syndrome
found in coal miners & in patients with variety of
pneumoconiosis
immunopathologic mechanism
inorganic dusts cause fibrosis as these can:
be directly cytotoxic
stimulate ROS
activate macrophages to produce cytokines & enhance
production of fibrogenic factors (i.e. TNF- a)
increase protease activity
increase inactivation of alpha-1 antitrypsin & leukocyte
elastase activity
 Berylliosis
Acute pneumonitis
Chronic granulomatous disease
o 2- 15 years of exposure
o occupational exposures:
manufacture of alloys, ceramics, high-
technology electronics, fluorescent lights
o PFT: normal or restrictive ventilatory pattern
o Dx:
open lung biopsy (granuloma formation similar to
sarcoidosis)
Tissue levels of beryllium
 Other inorganic dusts
Nuisance dusts
reduction in visibilty
irritation of eyes, ears, nasal passages, other
mucus membranes
dont affect architecture of terminal bronchioles or
acinar spaces nor destroy collagen
PFT: normal
CXR: radiodense dusts may produce radiographic
picture
Iron & iron oxide (siderosis)
Tin oxide (stannosis)
Barium sulfate (baritosis)
Lung diseases caused by organic
dusts
 Byssinosis
exposure to cotton dust
occupational exposures:
production of yarn for cotton, linen, rope making
treatment of cotton prior to spinning
occasional (early stage) & then regular (late
stage) chest tightness toward end of first
day of workweek- Monday chest tightness
progressive in 10- 25% of cases with chest
tightness recurring/ persisting throughout
workweek
 Byssinosis
PFT: obstructive ventilatory pattern
cotton dust exposure & cigarette
smoking with additive effect
Treatment:
bronchodilators
anti-histamines

reduction of dust exposure

 Grain dust
Occupational exposures:
Work in grain elevators
Work in flour/ feed mills

Symptoms: persistent cough, mucus

hypersecretion, wheeze,
dyspnea
PFT: reduced FEV1
reduced FEV1/ FVC
Grain dust exposure & cigarette
smoking with additive effect
 Farmers lung
exposure to moldy hay containing
spores of thermophilic actinomycetes
that produce hypersensitivity
pneumonitis
Acute: 4- 8 hours after exposure
fever, chills, malaise, cough,
dyspnea
Chronic: repeated attacks after similar
exposure
 Toxic chemicals
generally involves gases & vapors
toxic agents can produce acute & sometimes
life-threatening reactions in lung
affect lower airways & disrupt alveolar
architecture

smoke inhalation- carbon monoxide

poisoning with significant hypoxemia &
exposure to particulate smoke of fire fighters
& fire victims
repeated episodes of smoke inhalation
increase airway responsiveness
 Toxic chemicals
agents used in making synthetic materials
(i.e. isocyanates, aromatic amines,
aldehydes) cause chronic productive
cough, asthma, malaise, episodes of low-
grade fever
fluoropolymers when heated become
volatilized & cause fever, chills, malaise,
mild wheezing (polymer fume fever or meat
wrappers asthma)
fumes/ smoke of zinc, copper, magnesium,
other metals cause self- limited, influenza-
like syndrome
Environmental respiratory carcinogens

Agent Cancer
nickel nasal sinus & lung
cancer
vinyl chloride angiosarcoma of liver
wood/ wood adenocarcinoma of nose
finishing products
isopropyl oil nasal sinus cancer

Other proven/ suspected respiratory carcinogens:

acrylonitrile chromium
arsenic compounds polycyclic
hydrocarbons
beryllium (animal studies) iron oxide
bis (chloromethyl) ether mustard gas
talc uranium
 Assessment of disability
Physician has to assess:

Degree to which symptoms are related to

work or other environmental exposures
~ requires detailed work history

Severity of symptoms
~ requires objective assessment
 Assessment of disability
Objective assessment of severity of
symptoms
PFTs
Spirometry
Lung volume measurement
Diffusing capacity
Tests measuring airways hyperactivity
Determination of O2 saturation

may have to do tests after modest exercise

may have to do serial PFTs while patient is
at work environment

Physician determines degree of

 Assessment of disability
Data on the degree of impairment & its
relation to exposure can then be used
to set level of DISABILITY.
Different authorities may have
different guidelines & rules for setting
levels of disability.
Significant impairment may not always
mean significant disabilty.
Pneumonia
Vinci L. Urgel, M. D.
The symptoms of pneumonia were described by
Hippocrates (c. 460 BC380 BC):
Peripneumonia, and pleuritic affections, are
to be thus observed: If the fever be acute,
and if there be pains on either side, or in
both, and if expiration be if cough be
present, and the sputa expectorated be of a
blond or livid color, or likewise thin, frothy,
and florid, or having any other character
different from the common... When
pneumonia is at its height, the case is
beyond remedy if he is not purged, and it is
bad if he has dyspnoea, and urine that is
thin and acrid, and if sweats come out
about the neck and head, for such sweats
are bad, as proceeding from the
suffocation, rales, and the violence of the
disease which is obtaining the upper hand.
 Pneumonia
infection of the alveoli, distal airways, &
interstitium of lung manifested by increased
weight of the lung, replacement of lungs
sponginess by consolidation, & alveoli filled
with WBCs, RBCs, & fibrin

constellation of SSx (fever, chills, cough,

pleuritic chest pain, sputum production,
hyper- /hypothermia, increased RR, dullness
to percussion, bronchial breathing,
egophony, crackles, wheezes, pleural friction
rub) in combination with at least 1 opacity on
CXR
Normal lung

Lung tissue
in person
with pneumonia
Host defenses protecting the lungs
Innate (non- specific) defense
anatomical features of upper airways
glottis
cough mechanism
macrophages, fibronectin, lysozymes,
lactoferrin, IgG, defensins, cathelicidins,
collectins, complement
epithelial cells
Acquired (specific) defense
require T cell activation
specifically target offending pathogen
lymphocyte & mononuclear phagocytes
 Pathogenesis

Routes of infection
Gross aspiration
Microaspiration
Aerosolization
Hematogenous
spread
Direct spread
Microaspiration

Gross aspiration
Aerosolization
Hematogenous spread
 Contiguous spread

Empyema thoracis
 Factors in pathogenesis
Microbial factors
Ciliostatic factor- Chlamydia pneumoniae
Shear off cilia- Mycoplasma pneumoniae
Reduce tracheal mucus velocity- influenza virus
Proteases that split secretory IgA- Streptococcus
pneumoniae, Neisseria meningitidis
Capsule inhibits phagocytosis- S. pneumoniae
Resistance to microbicidal activity of phagocytes-
Mycobacterium, Nocardia, Legionella
Pneumolysin, neuroaminidase, hyaluronidase, IgA 1
protease
 Factors in pathogenesis
Host factors
Impaired host defense
hypogammaglobulinemia
defects in phagocytosis or ciliary
function
reduced CD4+ T lymphocyte counts
Genetic factors
polymorphism in or near TNF- a gene
Functional or anatomical asplenia
 Pathophysiology
VC, lung compliance, FRC, TLC less
than normal
Ventilation- perfusion mismatch &
intrapulmonary shunting are main
causes of hypoxemia
 Pathology
4 General patterns Bronchopneumonia

Lobar pneumonia
4 Stages:
congestion
red hepatization
gray hepatization
resolution

Bronchopneumonia
Interstitial
pneumonia
Miliary pneumonia
 Pulmonary complications

Necrotizing pneumonia
Abscess formation
Pulmonary infarction
Cavitation
Empyema/ bronchopleural
fistula
Community- acquired pneumonia
(CAP)
 CAP

Risk factors:
alcoholism
asthma
immunosuppression
age > 70 years
 CAP
Risk factors for pneumococcal disease:
dementia tobacco smoking
seizures alcoholism
CHF COPD
CVD

Risk factors for invasive pneumococcal disease:

male gender current tobacco smoking
black race passive exposure to tobacco
chronic illness smoke
 CAP
Risk factors for Legionnaires disease:
male gender current tobacco smoking
diabetes HIV infection
cancer hematologic malignancy
ESRD

Risk factors for gram- negative pneumonia:

aspiration previous hospitalization
bronchiectasis previous antibiotic treatment
alcoholism
 CAP
Etiology
culture
blood, sputum, pleural fluid, pulmonary tissue,
endobronchial secretions (via bronchial brush,
lavage)
IgM response
4X rise in Ab titer
Ag in urine, serum, pleural fluid
amplification of DNA/ RNA of respiratory
pathogen
 CAP
Clinical manifestations
severity from mild to fulminant, fatal
onset may be sudden & dramatic or
insidious
Symptoms:
fever headache
cough nausea & vomiting
pleuritic chest pain diarrhea
chills/ rigors myalgia
shortness of breath arthralgia
fatigue
 CAP
Signs
tachypnea
dullness to percussion
increased tactile & vocal
fremitus
egophony
whispering pectoriloquy
crackles
pleural friction rub
 CAP
Diagnosis of pneumonia based on PE
Sensitivity: 47- 69%
Specificity: 58- 75%

Clinical diagnosis of pneumonia should

be confirmed by CXR
 CAP
Severity of pneumonia
RR > 30/ min - single most useful sign of
severity
BTS Rule
ATS Definition
PORT Study
Causative organism:
P. aeruginosa, Klebsiella spp., E. coli, S.
aureus,
Acinetobacter spp.
 CAP
British Thoracic Society Rule for Definition of Severe CAP:
Confusion
Urea: > 7 mmol/L
RR: > 30/ min
BP: diastolic < 60 mmHg or systolic < 90 mmHg

American Thoracic Society Definition of Severe Pneumonia

Category Criteria
Major need for mechanical ventilation
requirement for vasopressors > 4
hours

Minor systolic BP < 90 mmHg

PaO2/ FIO2 < 250
multilobar involvement
Mortality Rate at 30 days among patients
with CAP, According to PORT Risk Class
% Mortality
Risk Class Criteria Outpatient
Inpatient

I Age < 50 yrs 0 0.5

No existing illness
or VS abnormality
II 70 pts 0.4 0.9
III 71- 90 pts 0
1.25
IV 91- 130 pts 12.5 9.0
V 131 pts NA 27.1
Mean 0.6 8.0
 CAP
Diagnosis
Chest radiography
High- resolution CT

Etiologic diagnosis
Blood culture
Sputum stains & culture
Grams stain- correlate culture results with this
KOH stain
AFB stain
Monoclonal antibody staining
Sputum suitable for culture:
> 25 WBCs/ LPF
< 10 squamous epithelial cells/ LPF
 CAP
Etiologic diagnosis
Detection of Ag in urine
use ELISA- L. pneumophila, S. pneumoniae
Serology
IgM Ab
4-x rise in titer of Ab to particular agent (convalescent vs.
acute- phase serum samples)- M. pneumoniae, C.
pneumoniae, Legionella spp., influenza virus A
Tests: complement fixation
indirect immunofluorescence
ELISA
Polymerase chain reaction
amplification of DNA or RNA of microorganisms
Legionella spp., M. pneumoniae, C. pneumoniae
Etiology in selected, recent series of CAP patients
from selected Asian-Pacific countries
S. pneumoniae
S. aureus
Anaerobes
17.15% G (-) rods
H. influenzae
40.92% K. pneumoniae
P. aeruginosa
M. pneumoniae
8.49%
C. pneumoniae
Legionella spp.
Others
Unknown

Atypical pathogens (13.24%)

Martinez FJ. Inf Dis Infoalert
 CAP
Treatment
 2007 IDSA/ ATS
Consensus Guidelines
on the Management of
Community-acquired
Pneumonia in Adults
2007 IDSA/ATS Consensus Guidelines on the
Management of CAP in Adults
Outpatient Treatment
POTENTIAL PATHOGENS
Streptococcus pneumoniae
Mycoplasma pneumoniae
Haemophilus influenzae
Chlamydia pneumoniae
Respiratory viruses
EMPIRIC THERAPY
Previously healthy & no use of
antibiotics w/in 3 mos:
macrolide (i.e. clarithromycin)-
level I
doxycycline- level III
With stable comorbid illness,
alcoholism, malignancies,
asplenia, immunosuppressing
conditions or use of
immunosuppressives, use of
antibiotics w/in past 3 mos:
respiratory FQ- level I
Beta-lactam (amox, amoxyclav,
ceftriax, cefpodox, cefurox) +
macrolide- level I
2007 IDSA/ATS Consensus Guidelines on
the Management of CAP in Adults

Outpatient Treatment

In regions with high rates (>25%) of infection with high-level

(MIC > 16 ug/mL) macrolide-resistant Streptococcus pneumoniae:
respiratory FQ- level III
Beta-lactam + doxycycline- level III
2007 IDSA/ATS Consensus Guidelines on the
Management of CAP in Adults

Inpatient, non-ICU Treatment

POTENTIAL PATHOGENS EMPIRIC THERAPY

Streptococcus pneumoniae respiratory FQ- level I

Mycoplasma pneumoniae beta-lactam (cefotax, ceftriax,
Chlamydia pneumoniae ampi, ertapenem) +
Haemophilus influenzae macrolide- level I
Legionella species (or doxycycline- level III)
Anaerobes (among those with
risk of aspiration)
Respiratory viruses
2007 IDSA/ATS Consensus Guidelines
on the Management of CAP in Adults
Inpatient, ICU Treatment
POTENTIAL PATHOGEN EMPIRIC THERAPY
Streptococcus pneumoniae Beta-lactam (cefotaxime,
Staphylococcus aureus ceftriaxone, sultamicillin)
Legionella species +
Gram-negative bacilli azithromycin- level II or
Haemophilus influenzae respiratory FQ- level I

for penicillin-allergic patients:

respiratory FQ + aztreonam
2007 IDSA/ATS Consensus Guidelines on
the Management of CAP in Adults
Special Concerns
If Pseudomonas is a consideration:
anti-pneumococcal, antipseudomonal Beta-lactam
(piperacillin-tazobactam, cefepime, imipenem, meropenem)
+
ciprofloxacin or levofloxacin (750 mg) or
aminoglycoside + azithromycin/ respiratory FQ

for penicillin-allergic patients:

aztreonam in lieu of Beta-lactam

(level III)
2007 IDSA/ATS Consensus Guidelines on
the Management of CAP in Adults

If community-acquired MRSA is a
consideration:
add vancomycin or linezolid
(level III)
 Algorithm for the managementoriented risk
stratification of CAP among immunocompetent adults
CAP

Any of the following:

1. RR > 30/min
2. PR > 125/min
3. Temp. > 40oC or < 36oC YES
4. SBP < 90mmHg or DBP < 60mmHg
5. Altered mental status of acute onset
6. Suspected aspiration
7. Unstable co-morbid conditions
8. Chest x-ray: multilobar, pleural effusion, abscess
NO
Low-risk CAP

Outpatient
Algorithm for the management oriented risk stratification
of CAP among immunocompetent adults

Any of the following:

YES 1. Severe sepsis & YES
septic shock High-risk CAP
2. Need for mechanical
ventilation

NO
ICU Admission
Moderate-risk
CAP

Ward Admission
 Empiric antibacterial therapy for CAP
Risk Stratification Potential Pathogen Empiric Therapy
Low-risk CAP Streptococcus pneumoniae Previously healthy:
Extended macrolides:
Haemophilus influenzae Amoxicillin
Oral nd
2 gen cephalosporin:
Clarithromycin
Chlamydia pneumoniae OR
Azithromycin
Cefaclor
Mycoplasma dihydrate
pneumoniae Extended macrolide
Cefuroxime axetil
Moraxella catarrhalis (suspected atypical
Enteric gram-negative bacilli pathogen)
Oral b-lactam/b-lactamase
(among those with co-morbid With stable co-morbid
inhibitor combination
illness) (BLIC): illness:
b-lactam/BLI combination
Amoxicillin-clavulanic acid (BLIC) or 2nd gen oral
Amoxicillin-sulbactam cephalosporin +/-
Oral 3rd gen cephalosporin:
Sultamicillin extended macrolide
Cefdinir Alternative:
Cefixime 3rd gen oral cephalosporin
Cefpodoxime proxetil +/- extended macrolide
 Empiric antibacterial therapy for CAP
IV non-antipseudomonal b-lactam:Pathogen
Risk Stratification Potential Empiric Therapy
- BLIC: amoxicillin-clavulanic
Moderate-risk CAP acid
Streptococcus pneumoniae IV non-antipseudomonal
ampicillin-sulbactam Haemophilus influenzae b-lactam (BLIC,
- cephalosporin: Chlamydia pneumoniae cephalosporin, or
carbapenem)
cefotiam Mycoplasma pneumoniae
cefoxitin Moraxella catarrhalis +
cefuroxime Na Enteric Gram-negative bacilli extended macrolide or
cefotaxime Legionella pneumophila respiratory fluoroquinolone
ceftizoxime Anaerobes (among those with (FQ)
ceftriaxone risk of aspiration)
- carbapenem: ertapenem
Respiratory fluoroquinolones:
Levofloxacin
Moxifloxacin
 Empiric antibacterial therapy for CAP
Risk Stratification Potential Pathogen Empiric Therapy
IV non-antipseudomonal b-lactam:
High-risk CAP Streptococcus pneumoniae No risk for P. aeruginosa:
- BLIC: amoxicillin-clavulanic
IV antipneumococcal,acid
Haemophilus influenzae IV non-antipseudomonal b-lactam
ampicillin-sulbactam
antipseudomonal
- cephalosporin:
b-lactam:
Chlamydia pneumoniae (BLIC, cephalosporin, or
carbapenem)
- BLIC: cefoperazone-sulbactam
Mycoplasma pneumoniae
cefotiam +
piperacillin-tazobactam
Moraxella catarrhalis
cefoxitin IV extended macrolide or
ticarcillin-clavulanic acid bacilli
Enteric Gram-negative
cefuroxime Na IV respiratory FQ
- cephalosporin:Legionella pneumophila
cefotaxime Anaerobes (among those With risk for P. aeruginosa:
cefepime
ceftizoxime with risk of aspiration) IV antipneumococcal
cefpirome antipseudomonal b-lactam (BLIC,
ceftriaxone Staphylococcus aureus
- carbapenem: cephalosporin, or carbapenem) +
Aminoglycosides:
- carbapenem: ertapenem Pseudomonas aeruginosa IV extended macrolide +
imipenem-cilastatin
Gentamicin
aminoglycoside
meropenem
Tobramycin
OR
doripenem
Netilmicin
IV antipneumococcal
Amikacin
antipseudomonal b-lactam (BLIC,
cephalosporin, or carbapenem) +
IV ciprofloxacin/levofloxacin (high
dose)
Usual recommended dosages of antibiotics in 50 to 60-kg
adults with normal liver and renal functions
Usual recommended dosages of antibiotics in 50 to 60-kg
adults with normal liver and renal functions
 CAP in Long-term-care facilities
pneumonia is leading cause of infection requiring
transfer of nursing residents to hospital

Risk factors for pneumonia in LTCFs:

profound disability male gender
bedridden state difficulty swallowing
urinary incontinence inability to take oral medications

Risk factors for aspiration pneumonia in LTCFs:

malnutrition contractures
tube feedings use of benzodiazepines &
hyperextended neck anticholinergic medicines
 CAP in LTCFs

Most common etiologic

agents:
S. aureus
aerobic gram-negative bacilli
S. pneumoniae
M. tuberculosis

anaerobic bacteria
 CAP in LTCFs

clinical presentation
insidious or nonspecific deterioration
in general health &/ or activity level
increase in RR to > 28/min is usually
the first manifestation
 CAP in LTCFs
Criteria for treatment in Nursing Home
RR < 30/ min
sO2 > 92%, room air
pulse rate < 90/min
temperature 36.5o C- 38.1o C
systolic & diastolic BP w/in 10 mm Hg of usual
readings
no feeding tube present
patient conscious
availability of medical & nursing care
wishes of patient & family
 Severe CAP

pneumonia requiring admission to ICU

mechanical ventilator commonly used
Other treatment modalities:
positioning of patient
use of cyclooxygenase inhibitors

use of aerosolized prostacycline or nitric

oxide
Aspiration pneumonitis/ pneumonia

introduction of foreign objects or

substances into LRT
commonly involves most dependent
areas in supine position- posterior
segments of upper lobes & superior
segments of lower lobes
Aspiration pneumonia/ pneumonitis
Etiologic agents:
Enterobacteriaceae, S. aureus, S. pneumoniae, H.
influenzae
2 clinical entities:
Aspiration pneumonitis- gastric contents
aspirated into lungs
Aspiration pneumonia- oropharyngeal flora
aspirated into lungs
Risk factors:
altered level of consciousness
incompetent gastroesophageal junction
elevated intragastric pressure or volume
neuromuscular disease that interfere with glottic
closure
 HOSPITAL-ACQUIRED
(Nosocomial or
healthcare-associated)
PNEUMONIA
 HAP
pneumonia occurring > 48 hours after
hospital admission & not incubating at time
of admission
2nd most common nosocomial infection
incidence is highest among intubated
patients in ICU
Ventilator- acquired pneumonia (VAP)-
pneumonia occurring > 48 hours of
mechanical ventilation & not incubating at
time of intubation
 HAP

Crude mortality rates: 30- 70%

Highest mortality rate among bacteremic
patients, patients infected with high- risk
pathogens, ICU patients

Risk factors for death in ICU:

shock ultimately/ rapidly fatal underlying disease
coma respiratory failure
ARDS high APACHE score
SIRS bilateral lung infiltrates on CXR
 HAP
Pathogenesis
Risk factors:
endotracheal intubation
enteral feeding
poor infection- control measures
prolonged use of inappropriate
antimicrobial agents
elevation in gastric pH ( by antacids, H2
antagonists, enteral gastric feeding)
 HAP
Etiology
64% of microorganisms isolated from lungs of
patients with nosocomial pneumonia were gram-
negative bacilli
P. aeruginosa, Acinetobacter, Enterobacter, K.
pneumoniae
S. aureus
S. pneumoniae
H. influenzae

plasmid-mediated ESBL (in Enterobacteriaceae)

plasmid-mediated carbapenemases
 HAP
Onset of HAP
Early-onset: < 5 days after admission,
core pathogens
Late-onset: > 5 days after admission,
resistant organisms
MRSA
Acinetobacter calcoaceticus-baumannii
Stenotrophomonas maltophilia
ESBL-producing Enterobacteriaceae
 HAP
Clinical manifestations
Presence of new or progressive infiltrates
on CXR + at least 2 of ff:
fever (> 37.8oC)
leukocytosis > 10,000 WBC/uL
production of purulent sputum
Other findings: dyspnea, hypoxemia,
pleuritic chest pain
Exclude noninfectious causes of lung
infiltrates
 HAP
Diagnosis
one of most controversial areas in management of HAP
invasive diagnostic testing
Endotracheal aspiration
PSB or BAL sampling via FOB
Blinded invasive methods (blinded bronchial sampling, mini-BAL,
blinded PSB)
PSB: > 103 CFU of bacteria per brush
BAL: > 104 CFU of bacteria per ml lavage fluid
pellet of centrifuged BAL fluid: 1% or 5% of WBC w/
intracellular bacteria
 HAP
Treatment
 Healthcare-associated Pneumonia
hospitalized in an acute care hospital for > 2
days within 90 days of the infection
resided in a nursing home or long-term care
facility
received recent IV antibiotic therapy,
chemotherapy, or wound care within past 30
days of the current infection
attended a hospital or hemodialysis clinic
Thank you very much!
Acute Respiratory
Distress Syndrome
(ARDS)
Vinci L. Urgel,
M.D.
 ARDS

clinicalsyndrome of severe dyspnea of

rapid onset, hypoxemia, & diffuse
pulmonary infiltrates leading to
respiratory failure
 ARDS
caused by diffuse lung injury from many
underlying medical & surgical disorders
increased risk of developing ARDS if with >
1 predisposing condition
 ARDS
Direct lung injury
Pneumonia
Aspiration of gastric contents

Pulmonary contussion

Near-drowning

Toxic inhalation injury

 ARDS
Indirect lung injury
Sepsis
Severe trauma (multiple bone fractures,
flail chest, head trauma, burns)
Multiple transfusions
Drug overdose

Pancreatitis

Post-cardiopulmonary bypass
 ARDS
Other clinical variables associated with
development of ARDS
Older age
Chronic alcohol abuse
Metabolic acidosis
Severity of critical illness
APACHE II score (compared to those with < 9)
> 16 with 2.5X increase in risk
> 20 with > 3X increase in risk
 Diagnostic criteria
Oxygenation Onset Chest Xray Absence of LA HPN
PaO2/FIO2
ALI < 300 mmHg Acute Bilateral alveolar or PCWP < 18 mmHg or
interstitial infiltrates no clinical evidence of
increased LA pressure
ARDS < 200 mmHg Acute Bilateral alveolar or PCWP < 18 mmHg or
interstitial infiltrates no clinical evidence of
increased LA pressure
 ARDS
PaO2/ FIO2 < 200 mm Hg

ALI
PaO2/ FIO2 < 300 mm Hg
Clinical Course &

Pathophysiology
 Phases of ARDS

Exudative phase
Proliferative phase

Fibrotic phase
 Exudative Phase
alveolar capillary endothelial cells & type I
pneumocytes injured
loss of normally tight alveolar barrier to fluid &
macromolecules
edema fluid rich in protein accumulates in
interstitial & alveolar spaces
significant concentrations of cytokines & lipid
mediators in the lung
neutrophils go into lung interstitium & alveoli
hyaline membrane whorls form
vascular obliteration by microthrombi &
fibrocellular proliferation
 Exudative Phase
alveolar edema predominantly in dependent
portions of lung atelectasis decreased
lung compliance
intrapulmonary shunting hypoxemia
hypoxemia
increased work of breathing
microvascular occlusion reduced blood
flow to ventilated portions increased dead
space, pulmonary hypertension hypercapnia
 Exudative Phase
encompasses first 7 days of illness after exposure to
a precipitating ARDS risk factor
symptoms usually present within 12- 36 hours after
initial insult (can be delayed by 5- 7 days)
rapid shallow breathing, inability to get enough air
tachypnea + increased work of breathing
respiratory fatigue respiratory failure
Laboratory results generally nonspecific
CXR: alveolar & interstitial opacities > of LFs
similar to cardiogenic pulmo edema but rarely with cardiomegaly, pleural
effusions, pulmo vascular redistribution
CT Scan: extensive heterogeneity of lung involvement
 Exudative Phase

early features of ARDS & ALI nonspecific

Differential diagnoses
cardiogenic pulmonary edema
diffuse pneumonia

alveolar hemorrhage

acute interstitial lung disease

acute immunologic injury

toxin injury

neurogenic pulmonary edema

 Proliferative phase
usually last from day 7 to day 21
period of recovery & liberation from mechanical
ventilation
many still with dyspnea, tachypnea, hypoxemia
some develop progressive lung injury & early
changes of pulmonary fibrosis
histologic signs of resolution:
initiation of repair, organization of alveolar exudates, shift
from neutrophil to lymphocyte-predominant pulmonary
infiltrate
proliferation of type II pneumocytes along alveolar basement
membranes synthesize new surfactant & differentiate into
type I pneumocytes
 Fibrotic phase
many patients recover lung function 3- 4 weeks after initial
pulmonary injury
alveolar edema & inflammatory exudates converted to
extensive ductal & interstitial fibrosis
acinar architecture is disrupted emphysema-like changes
with large bullae
intimal fibroproliferation in pulmo microcirculation
progressive vascular occlusion pulmonary hypertension
increased risk of pneumothorax
reduced lung compliance
increased pulmonary dead space
patients burdened with excess morbidity
may require long-term support on MV &/or supplemental
oxygen
lung biopsy evidence of pulmonary fibrosis mortality
 Time course for development &
resolution of ARDS
Exudative Proliferative Fibrotic

Edema Hyaline Interstital inflammation Fibrosis

Membranes Interstitial fibrosis

0 2 7 14 21. . .
Day
 Treatment
reductions in ARDS/ALI mortality are largely
the result of general advances in the care of
critically ill patients
General principles of management:
recognize & treat underlying medical & surgical
disorders
minimize procedures & their complications
do prophylaxis against venous thromboembolism, GI
bleeding, central venous catheter infections
promptly recognize nosocomial infections
provide adequate nutrition
 Prevention of alveolar collapse
Positive end-expiratory pressure (PEEP)
significant alveolar collapse can occur at end-expiration
reduced oxygenation
minimize FIO2
maximize Pa
O2
Optimal PEEP for alveolar recruitment
12- 15 mm Hg
lower inflection point on pressure-volume curve
(represents alveolar opening)
~ titrate PEEP to lower inflection point keep lung
open
 Pressure-volume relationships of
lungs of patient with ARDS
Alveoli

500
Upper inflection point
Volume, mL

250

Lower inflection point

0 15 30 45
Pressure, cmH2O
 Management of Mechanical
Ventilation
mechanical ventilation can aggravate injury
resulting from:
repeated alveolar overdistension
recurrent alveolar collapse
attempts to fully inflate consolidated lung may lead
to overdistension & injury to more normal areas
use of low TV would protect against ventilator-
induced lung injury
ARDS Network Trial
low TV (6 ml/KBW) vs. conventional TV (12 ml/KBW)
lower mortality with low TV (31% vs. 40%)
 Improvement of Oxygenation
Inverse ratio ventilation
increase mean airway pressure
Inspiratory time lengthened to make it longer than
Expiratory time (I : E > 1 : 1)
diminished time to exhale dynamic hyperinflation
increased end-expiratory pressure
lower peak pressures than conventional ventilation

no mortality benefit demonstrated

Prone position
uncertain effect on clinical outcomes
 Other strategies in mechanical
ventilation
High-frequency ventilation (HFV)
RR 5-20 cycles/second & low TV (1-2 ml/KBW)
Extracorporeal membrane oxygenation
(ECMO)
clear survival benefit in neonatal RDS but not ARDS
Partial liquid ventilation (PLV)
Perfluorocarbon (inert high-density liquid that easily
dissolves O2 & CO2)
no survival benefit
 Fluid Management
increased extravascular lung water
impaired vascular integrity
increased LA pressure

fluid restriction & diuretics

reduce LA filling pressures minimize pulmonary
edema
prevents further decrease in arterial oxygenation & lung
compliance
improves pulmonary mechanics

shortens ICU stay & duration of MV

watch out for hypotension & hypoperfusion of

critical organs
 Glucocorticoids
ARDS: abundant inflammatory mediators &
leukocytes
treatment at early or late ARDS: few studies show
any benefit
current evidence doesnt support use in early
ARDS
if without improvement after 1 week of supportive
therapy empirical trial to speed up resolution of
ARDS
 Other Therapies

Surfactant

Inhaled NO
improve oxygenation
no significant improvement in survival or
decrement in time on MV
 Evidence-based Recommendations for
ARDS Therapies
Treatment Recommendation
Mechanical Ventilation
Low TV A
High-PEEP or open-lung C
Prone position C
HFV & ECMO D
Minimize LA filling pressures B
Glucocorticoids C
Surfactant replacement, inhaled NO D
& other anti-inflammatory therapy
(e.g. ketoconazole, PGE1, NSAIDs)