Medicine 5.1 LECTURER: Dr.

Zotomayor
PNEUMONIA DATE: Jan. 06, 2015

OUTLINE Based on the Philippine CAP guidelines, this patient is considered as a low-risk
I. Sample Cases CAP who is previously healthy. There is no such thing as a healthy smoker.
Amoxicillin is the treatment of choice for this case.
II. Anatomy and Physiology
III. Main Function of the Respiratory system
ANATOMY AND PHYSIOLOGY
IV. Pathogenesis of Pneumonia
V. Routes of Transmission
VI. Pathophysiology
VII. Pneumonia
VIII. Community Acquired Pneumonia
IX. HAP, VAP, HCAP

References
1. Powerpoint lecture
2. Recording in ITALICS

SAMPLE CASES
1. A 24 y.o. male is consulting because of cough and dyspnea of 10 days
duration. Chest exam reveals bibasal crackles and wheezes. Chest x-ray
shows clear lung fields. The diagnosis is:
A. Pneumonia
B. Lung abscess
C. Acute bronchitis
D. Upper respiratory infection
Since it was given from the question that there are no infiltrates, pneumonia is
eliminated.Pneumonia and lung abscess will show abnormal x-ray findings.Upper
airway infection is also eliminated since chest exam reveals bibasal crackles and
wheezes. Acute bronchitis is the answer since it mimics the infection of the
lower respiratory tract but does not show any consolidation.

2. A 70 year old male smoker is hospitalized for fever, cough and dyspnea,
history reveals that the patient has not received any form of treatment
during the last year. Initial chest x-ray only shows hyperaeration
consistent with emphysema. Twelve hours after admission, he is
intubated for increasing dyspnea and is placed on mechanical
ventilation. Repeat chest x-ray one hour after intubation now shows
right lower lobe opacification with air bronchogram. He has: Figure 1. Respiratory Tree
A. Community-acquired pneumonia (CAP)
B. Hospital acquired pneumonia (HAP) The main function of our respiratory tree is to protect us from harmful
C. Ventilator-associated pneumonia (VAP) particles and microorganisms that are in the air that we breathe.
D. Health-care associated pneumonia (HCAP) The larynx and vocal cords prevents aspiration through the gag and
This is a typical presentation of a patient whose chronological presentation tells cough reflexes.
you what is going on. Initial x-ray: because this is a smoker, he probably has
COPD. This is hyperaeration consistent with emphysema; remember that
hyperaeration does not involve the presence of infiltrates. Repeat x-ray of right
lower lobe opacification with air bronchogram, indicates presence of an air space
consolidation that is compatible with pneumonia. The primary diagnosis would
probably be COPD in acute exacerbation. But there is another component to his
problem, and this is what is being asked of you.
The acuteness of the development of signs and symptoms and the tests which
are initially normal may be too soon to be able to tell you the abnormality. The
Pneumonia that you saw after 13 hours of admission is likely an incubating
community acquired pneumonia. Other choices are also eliminated since the
patient has no recent hospital admission and usually the other choices occur
after 48 hours of admission.

3. A 32 year old male, smoker from pasig city, is consulting for fever and Figure 2. Lining of the airways, ciliated epithelium of the trachea
cough of 4 days duration. He has no co-morbidities. He also has no Mucus is continuously swept into the throat. All of the collected
recent antibiotic intake. Chest x-ray shows left lower lobe pneumonia. particles including inanimate objects may be filtered and trapped in this
VS are BP 124/80 HR 94 RR 24 and Te,p 38.3C. He is conscious and mucus apparatus and moved to the throat, or may be expectorated or
coherent. Based on the local guidelines, the antibiotic of choice is: swallowed.
A. Cefixime Smokers respiratory flora is different from the flora of non smokers.
B. Amoxicillin The mucocillary apparatus is also affected for up to 6 to 8 hours per
C. Doxicycline cigarette stick which makes it dysfunctional, increasing the risk of
D. Co-amoxiclav developing lower respiratory tract infections including pneumonia.

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Alveolar macrophages, are recruited when foreign and harmful
organisms land on the alveoli and are very effective in elminating them.
However, some particles ingested by the macrophage do not always
result in the death of the organism. A good example would be
tuberculosis, where the bacilli are just neutralized.
MAIN FUNCTION OF THE RESPIRATORY SYSTEM
Obtain oxygen from external environment and supply it to the cells
Remove carbon dioxide produced by cellular metabolism from the body
OTHER FUNCTIONS
Phonation - production of sounds by the movement of air through the
vocal cords
Pulmonary defense mechanisms
Pulmonary metabolism and the handling of bioactive materials
PATHOGENESIS
Results from host response to proliferation of pathogens in the alveoli
Microbial Factors
Number of organisms
Virulence
Size of Inhaled Particle
Host Factors/ Defenses
Hair and turbinates of the nares - catch larger inhaled particles before
they reach the lower respiratory tract
Normal oropharyngeal flora - helps prevent the overflow of the more
virulent pathogens; Gram (-) pneumonia is a result of alteration in the
normal oropharygeal flora.
Gag and Cough Reflexes - protection from aspiration
Branching of the Tracheo-bronchial tree - traps particles on the airway
lining
Resident Alveolar Macrophages - extremely efficient at clearing and
killing pathogens; assisted by local proteins that have intrinsic
opsonizing properties or antibacterial/antiviral activity
Lymphatics- eliminates pathogens once engulfed by macrophages;
pathogens then no longer represent an infectious challenge
ROUTES OF TRANSMISSION
1. Aspiration of organisms that colonize the oropharynx
o The most common mechanism for the production of pneumonia
o Healthy individuals transiently harbor common pulmonary
pathogens in the nasopharynx; microaspiration occurs frequently
(e.g. during sleep) and more frequent ly when growing old (50s or
60s). And it is during this time that co-existing conditions normally
occur (hypertension, diabetes, smoking related like COPD,
malignancy)
o Organisms: S. pneumoniae, H. influenzae, M. catarrhalis,
anaerobes (gross aspiration), Enterobacteriaceae
2. Inhalation of Infectious Particles Chlamydia and mycoplasma
o Airborne droplet nuclei are small enough to bypass host defenses
in the upper respiratory tract and airways
o Include M. pneumoniae, C. pneumoniae, L. pnemophila
3. Hematogenous dissemination from extrapulmonary site
o In patients with bacterial endocarditis, IV catheter infections
(staphylococcus aureus) and extrapulmonary bacteremias (UTI and
soft tissue infection that gain access to the systemic circulation)
o Common in young individuals who developed infection of hair
follicles or skin structures of the face. During pimple manipulation,
there can be secondary infection of the skin that can gain access to
the vascular system and spread systemically. This is usually caused
by S. aureus, and instead of lobar consolidation, it will present with
Group 19 | Pio, Raph, Jobs, Nica, Pao
typical radiographic findings of multiple foci in the lungs at
different stages, and may also cause extrapulmonary bacteremia.
4. Direct inoculation or contiguous spread
o Tracheal intubation (oral flora) or stab wounds (skin flora)
o Adjacent infection from the mediastinum or subphrenic space.
A liver abcess that ruptured in the pleura or into the pleural space
and gained access to the circulation, may present with
hematogenous multiple foci; while a subphrenic abscess that
ruptured in the right lower thoracic cavity may manifest with focal
involvement mimicking a consolidation or a lung abscess..
o When the upper airway is bypassed because there is a need to
oxygenate or suction the lower respitary tree in an obtunded
patient, some defense mechanisms are also bypassed which is why
there is a need for adequate nursing care/ prevention of aspiration
of oral cavity secretions since this may trickle down the sides of the
ET tube and eventually reach the lower RT causing VAP.
o These are uncommon conditions and by history, you will have an
inkling that you are dealing with these conditions.
PATHOPHYSIOLOGY
Figure 3. Pathophysiology of Pneumonia.
Most of the manifestations of pneumonia are not related to the
organisms themselves, but to the hosts response to these pathogens.
Inflamatory cells that are present to control the infection and the
consequent inflammation that follows it causes the fever and purulent
phlegm; and in order to get rid of this we tend to cough.
If coughing is severe enough there is a tendency to become hypoxemic
and eventually alkalotic. Dyspnea may follow, and with a decrease in
lung compliance the labour of breathing becomes harder that
respiratory failure may occur.
At present, a new diagnostic technique is being introdueced where
procalcitonin, a marker created by the parathyroid glands, is used. This
substance is elevated in bacterial infections, and not in viral infections,
allowing the physician to distinguish between the two. This is important
in the formulation of a treatment plan. Most of the community
acquired pneumonias that are encountered are bacterial in origin, since
the viral ones can be self-limiting.
It is not being done here in the Philippines because the marker for pro
calcitonin itself is much more expensive than the course of the
antibiotics needed to treat the illness.
PNEUMONIA
Definition: an infection of the lung parenchyma
Classification
Community acquired pneumonia (CAP)
Healthcare associated pnemonia (HCAP)
Hospital acquired (Nosocomial) pneumonia
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o Ventilator associated pneumonia (it is a misnomer because it is 6. Tuberculosis, all forms 25,870 31.0 6.4
not due to the ventilator itself but because of the endotracheal 7. Ill-defined and unknown 21,278 25.5 5.3
tube.) Try to prevent the use of ventilators. causes
8. Chronic lower respiratory 18,975 22.7 -
diseases
9. Diabetes Mellitus 16,552 19.8 -
10. Perinatal causes 13,180 15.8 -

Figure 4. Pneumonia Spectrum: Implications on Pathogens and Outcome

The risk for multidrug resistant pathogens increases from CAP to HCAP
(transition between the two) to HAP, and VAP. When you have MDR
pathogen, diagnosis and appropriate treatment will be delayed
therefore morbidity and mortality of the patients also increases.
Epidemiology
Figure 6. After two years (2009), Pneumonia (purple) became the 4th cause of
mortality. In decreasing order: Diseases of the heart (blue), Diseases of the Vascular
system (red), Malignant neoplasms (yellow), Pneumonia (purple), and Accidents
(cyan).
A considerable proportion of patients with CAP require hospitalization
Pneumonia treatment in tertiary hospitals in the Philippines cost Php
64M for 3861 reimbursements
In 2010, Philhealth paid Php 2.042B (295,390 claims) for Pneumonia
highest among all cases claimed

Figure 5. Percentage of Hospital Mortality

CAP has 10% mortality rate and it doubles when you have HCAP (19.8),
then triples when you have VAP (29.3%).

Table 1. In terms of morbidity, Pneumonia is the number 1 cause in 2007

MORBIDITY: TOP TEN CAUSES
Number and Rate* -- 2007
2007
Diseases
Number Rate
1. Acute Lower Respiratory Tract 776, 562 929.4 Figure 7. LRTI is third leading cause of death worldwide. Pneumococcal pneumoniae
Infection and Pneumonia is the leading known cause of lower respiratory infection mortality. Streptococcus
pnuemoniae, most common strain.
2. Bronchitis/Bronchiolitis 719,982 861.6
3. Acute watery diarrhea 577,118 690.7 COMMUNITY ACQUIRED PNEUMONIA
4. Influenza 379,910 454.7 MICROBIAL CAUSES OF CAP
5. Hypertension 342,284 409.6 Typical Bacteria Atypical Bacteria
6. TB Respiratory 103,214 123.5
S. pneumonia M. pneumonia
7. Chickenpox 46,779 56.0
H. influenzae C. pneumonia
8. Diseases of the Heart 37,092 44.4
9. Malaria 19,894 23.8 Others (in selected cases): Legionella spp.
10. Dengue fever 15,838 19.0 o Staphylococcus aureus Respiratory viruses
o Gram- negative bacilli
Table 2. In terms of mortality, Pneumonia is the number 5 cause in 2007 o Anaerobes
MORTALITY: TOP TEN CAUSES
Number and Rate* -- 2007 S. pneumonia is the most common cause of CAP
2007 Mycobacterium should also be consideredwhen suspecting CAP in Asian
Causes countries
Number Rate %
Table 3. Commonly identified organisms in CAP in 8 Asian countries
1. Heart Disease 70,861 84.8 17.6
2. Vascular System Diseases 51,680 61.8 12.8 S. pneumoniae: Most Commonly identified Organism in CAP
(8 ASIAN Countries)
3. Malignant Neoplasms 40,524 48.5 10.1
4. Accidents** 34,483 41.3 8.6 Pathogen Isolated (N = 390) No. of Isolates (%)
5. Pneumonia 32,098 38.4 8.0 S. pneumoniae 114 (29.2)
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Klebsiella pneumoniae 60 (15.4) Moraxella catarrhalis, C.

Haemophilus influenza 59 (15.1) pneumoniae
Pseudomonas aeruginosa 26 (6.7) Structural Lung Disease P. aeruginosa, Burkholderia cepacia,
Staphylococcus aureus 19 (4.9) S. aureus
Mycobacterium tuberculosis 13 (3.3) Dementia, Stroke, Decreased level Oral anaerobes, gram negative
Moraxella catarrhalis 12 (3.1) of Consciousness enteric bacteria
Others 77 (19.7) Lung abscess CA-MRSA (Community Acquired),
oral anaerobes, endemic fungi, M.
Mycoplasma pneumoniae 61/556 (11.0)
tuberculosis, atypical mycobacteria
Chlamydia pneumoniae 55/411 (13.4)
Travel to Ohio or St. Lawrence River Histoplasma capsulatum
S. Pneumoniae contributes to a significant proportion of CAP regardless Valleys
of age
Travel to SW USA Hantavirus, Coccidioides spp.
S. Pneumoniae disproportionately affects those at the extremes of age
Travel to SEA Burkholderia pseudomallei, avian
Comorbidities increase all-cause pneumonia risk in adults.
influenza virus
Table 4. Microbial causes of CAP by site of care Stay in hotel or cruise ship in Legionella spp.
Microbial Causes of Community Acquired Pneumonia By Site of Care previous 2 weeks
Hospitalized Patients Local influenza activity Influenza virus, S. pneumoniae, S.
Outpatient Non-ICU ICU aureus
S. pneumoniae S. pneumoniae S. pneumoniae Exposure to bats or birds H. capsulatum
M. pneumoniae M. pneumoniae S. aureus Exposure to birds Chlamydophylia psittaci
H. influenzae C. pneumoniae Legionella spp. Exposure to rabbits Francisella tularensis
C. pneumoniae H. influenzae Gram-negativebacilli Exposure to sheep, goats, parturient Coxiella burnetti
Respiratory Viruses Legionella spp. H. influenzae cats
Respiratory Viruses
CLINICAL MANIFESTATIONS OF CAP
Respiratory viruses include influenza A and B, adenoviruses, Acute (to subacute) Course Hours to days to few weeks
respiratory syncytial viruses, and parainfluenza viruses.
Respiratory symptoms Any combination of cough, purule nt
Outpatient and Non-ICU patients almost have the same common
sputum, dyspnea, pleuritic chest pain
causes of CAP.
(signify inflammation of the parietal
For ICU patients, the organisms are different (but take note that the
pleura)
above table was from Harrisons which is North American and may not
reflect the organisms found in the Philippine ICU setting). Constitutional Symptoms Freque ntly fe ver; chills, headache,
Extrapulmonary M anifestations obtundation, diarrhea. In atypical
RISK FACTORS FOR CAP organism, can also manifest with GI
ETIOLOGY RISK FACTORS manifestations
CAP Alcoholism, asthma, COPD, CHF, CKD, Abnormal chest findings Consolidation, pleuritis +/- effusion,
immunosuppre ssion, rales, whe ezes
institutionalization, old age
Pneumococcus Tobacco smoking (number 1 cause), COPD CLINICAL DIAGNOSIS
Staphylococcus Viral infe ction, IV drug use Chest X-Ray
o Required for the diagnosis
Enterobacteriaceae Recent hospitalizations, recent
o Confirms the presence and location of infiltrates
antibiotic treatment, alcoholism
If normal consider tracheobronchitis
P. aeruginosa Structural lung disease, severe COPD, Lung abcessess indicates S. aureus as an etiologic agent
neutrope nia, systemic steroid use; recent o Assessment extent (severity)
use of antibiotics o Detects presence of effusion or cavitation
Legionella Diabetes, recent hote l stay or ship cruise, Consider when patient has pleural effusion since this can help
cell-mediated de ficiency decide whether to insert a chest tube
If multiple lobes are involve, this will show specific
Tobacco smoking of >10 pack years is especially high risk, but there is
radiographic presentation like cavitation which suggests the
no safe level of smoking.
presence of necrotizing pneumonia. If present, this should
Recent use of broad spectrum antibiotics within the last 3 months
warrant close monitoring since it may indicate rapid
because organism can develop reisistant patterns
deterioration.
Individuals who have a history of staying in a hotel or cruise ship are at If there is lung abscess, presence of air fluid level inside the
high risk for Legionella Pneumonia parenchymal structure is noted, and this tells you that the
patient is tremendously sick. It also tells you the possible
EPIDEMIOLOGIC FACTORS SUGGESTING POSSIBLE CAUSES OF CAP etiologic agent, as multiple abscesses is typical of a S. aureus
Factor Possible Pathogens infection.
Alcoholism S. pneumoniae, oral anaerobes, K. Cavitations in the apical segment may indicate Tuberculosis. If
pneumoniae, Acinectobacter spp., there are parenchymal infiltrates with a cavitary lesion in the
Mycobacterium tuberculosis middle of the chest which corresponds somehow to the apical
COPD and/or Smoking H. influenzae, P. aeruginosa, segment of the right lower lobe or left lower lobe, still
Legionella spp., S. pneumoniae, consider the possibility of TB.
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o Rules in/out other diagnosis
o May be normal in some situations
If the patient comes to you, and x-ray is done within the first
24-48 hours, result may still be normal and yet there are
adventitious sounds that tell you there is something there;
this is referred to as the radiographic lag phase. Consider
doing a repeat x-ray for the first 24-48 hour period, and then
you might be able to see it. It only occurs for 2% of all cases.
Recall case #2 where the patient sought consult for a COPD
exacerbation, xray was normal, and was then intubated 12
hours after. Repeat xray revealed an air bronchogram. Does
that make him hospital acquired pneumonia or ventilator
associated pneumonia? This is still considered community for diagnostic evaluation. (Right) Good sputum sample showing many WBCs
acquired pneumonia, because the patient was in the
incubation period at the time of admission.
Figure 8. Homogenous opacification just like the heart, will not allow x-rays to
penetrate or expose the film resulting in a radiopaque finding. Lung parenchyma is
mainly air, and it allows exposure of films therefore it turns black. This is present on
both the left and right lower lobes. The patient has bibasal pneumonia and PE findings
should support the presence of consolidation on both sides.
Figure 9. (Left) Chest X-Ray result showing consolidation of the right upper lobe and
bulging of the minor fissure. There are a lot of exudates present there. This is a
classical radiologic feature of Klebsiella pneumonia or Fried Landers bacillus. You also
have to consider co-existing TB or that the pneumonia was caused by TB (Right)
Pneumatocoele suggest Staphylococcal pneumonia in adult. In infant,
pneumatocoele, indicates healing process
ETIOLOGIC DIAGNOSIS
Sputum Examination 1.
o Gram Staining as performed initially indicates if sputum is good for 2.
culture 3.
o Low sensitivity and specificity
o Good sputum: < 10 Squamous epithelial cells (SEC) and > 25
PMNs per LPF, indicates specimen is from lower respiratory tract.
If there are abundant SEC, it means that the sample came from the
upper respiratory tract.
o May do sputum induction if no phlegm is produced
3% saline using ultrasonic nebulization
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Figure 10. (Left) Poor sputum specimen with abundant SECs under low
power. It suggests contamination with saliva and as a result cannot be used
and few SECs. Note presence of gram positive diplococci.
Other Diagnostic Tests
o 2 Blood Culture and Sensitivity (C/S) for some hospitalized
patients
In only very sick individuals, intubated, requiring ICU
admission, that is where some books would say blood cultures
would be indicated.
o Thoracentesis if (+) significant pleural effusion
Significant means on lateral decubitus film, there is 1cm
layering of the fluid to the top. This may suggest a
complicated parapneumonic effusion
Indicators of complicated effusion include: able to identify
organism by gram staining, with pus/purulent, very low pH.
Monitor effusion as in might not only require Watch that
thoracentesis but also insertion of a chest tube for drainage;
to control source of infection
o Urinary antigen tests for Legionella, Pneumococcus
It is a very high consideration. It is only able to identify 0-1,
accounts for the majority of the Legionella disease in the
clinics. It is sufficient enough. If it is negative, then you are not
dealing with Legionella.
o PCR for Legionella (research), Mycobacteria
AFB smear is still the preferred method of diagnosing MTB in
the Philippines.
o Serologic Test: for Mycoplasma, Chlamydia
This has an acute and convalescent phase, meaning a sample
should be taken now, and again after 4-6 weeks. This is done
to monitor patient recovery.
MANAGEMENT: ADULT CAP GUIDELINES
USA PHILIPPINES
ATS 1993 1998 (PSMD)
IDSA 1998 2004 (PSMD/PCCP/PAFP)
IDSA 2000 2010 (PSMD/PCCP/PAFP/PCR)
CDC 2000
ATS 2001
IDSA/ATS 2007
MANAGEMENT: SITE OF CARE
Outpatient
Medical Ward or Private Room
ICU
The purpose of this is to identify patients who can be treated on an
outpatient basis in order to minimize cost. 80-90% can be treated as an
outpatient while some require admission to a medical ward. 3-5% have
severe presentation requiring ICU admission.
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IDSA/ATS COMMUNITY ACQUIRED PNEUMONIA GUIDELINE OF 2007 71 90 Low III 2.8(6,790) Inpatient
Severity-of-illness scores, such as the CURB-65 Criteria (Confusion, (briefly)
Uremia, Respiratory Rate, Low Blood pressure, Age 65 or greater) or 91 130 Moderate IV 8.2(13,104) Inpatient
prognostic models, such as PSI,can be used to identify patients with > 130 High V 29.2(9,333) Inpatient
CAP who may be candidates for outpatient treatment.
Pneumonia Severity index
CURB-65 CRITERIA More comprehensive, more accurate
Confusion Takes into account co-existing units such as demographics and co-
Uremia/Increased BUN or creatinine morbid illness, abnormal PE findings and laboratory and radiographic
BUN > 7 mmol/L (20 mg/dl) findings.
Respiratory rate >30cpm Put together all the predictors and get the total score. If there are no
Low Blood pressure <90mmHg systolic, <60mmHg diastolic predictors, then you have a low risk. If the score is > 70, then the patient
Age 65 years or greater will be treated in the inpatient setting and will have a higher risk.
It allows you to classify patients into low, moderate and high risks and
Table 5. IDSA/ATS CAP Guidelines 2007 allows you to make a decision to admit patients
CURB-65
Score 30-day Mortality Rate Recommendation Objective criteria or scores should always be supplemented with physician
(%) determination of subjective factors, including the ability to safely and
0 0.7 Outpatient reliably take oral medication and the availability of outpatient support
1 2.1 Outpatient resources IDSA/ATS CAP Guidelines 2007
2 9.2 Ward
3 14.5 ICU CRITERIA FOR ICU ADMISSION (SEVERE CAP)
4 40 ICU Minor Criteria
5 57 ICU o RR > 30 breaths/min
30-day mortality rate in studies tell us that patients may be best treated o PaO2/FiO2 < 250
in an outpatient setting if their score is 0-1, wards with a score of 2, o Multilobar infiltrates
and ICU with scores of 3-5. Patients with scores of 3-5 will have a 15- o Confusion/disorientation
50% mortality rate. o Uremia (BUN level > 20mg/dL)
o Leukopenia ( WBC count < 4,000 cells/mm3)
Table 6. Pneumonia Severity Index o Thrombocytopenia (Platelet count < 100,000 cells/mm3)
Patient Characteristics Points o Hypothermia (Core temp < 36oC)
o Hypotension requiring aggressive fluid resuscitation
Demographics
Male Age in years Major Criteria
o Invasive mechanical ventilation
Female Age in years 10
o Septic shock with the need for vasopressors
Nursing home resident +10
*SEE APPENDIX FOR CAP RISK CLASSIFICATION AND SITE OF CARE DECISION
Comorbid illness
Neoplastic disease +30
Management: Antibiotic Therapy
Liver disease +20
Until more accurate and rapid diagnostic methods are available, the
Congestive Heart Failure +10
initial treatment for most patients will remain empirical (IDSA/ATS CAP
Cerebrovascular disease +10
Guidelines 2007)
Renal disease +10
Antibiotics Classes Used in Bacterial Pneumonia:
Physical Examination Findings o Beta-lactams more commonly used
Altered mental status +20 Penicillins - prototype
Respiratory rate > 30 breaths per minute +20 Narrow spectrum: PCN-G, Phenoxymethylpenicillin
Systolic blood pressure < 90mmHg +20 (these drugs are directed against gram-positive
Temperature < 35oC or > 40OC +15 organisms)
Pulse rate > 125 beats/min +10 Anti-staphylococcal: Methicillin (not available locally),
Laboratory and Radiographic findings Oxacillin (used for methicillin resistant staphylococcus
Arterial pH < 7.35 +30 aureus), Cloxacillin, Nafcillin
BUN > 64 mg/dL (22.85 mmol/L) +20 Extended-spectrum:
Sodium < 130mEq per liter (130 mmol/L) +20 - Aminopenicillins: Ampicillin, Amoxicillin
Glucose > 250 mg/dL (13.87mmol/L) +10 - Anti-Pseudomonal: Ticarcillin, Piperacillin (can be
Hematocrit < 30% +10 combined with Tazobactam to become Tazocin)
pO2 < 60 mmHg or O2Sat < 90 mmHg +10 Combined with Beta-Lactamase Inhibitors: Coamoxiclav,
Pleural effusion +10 Ampicillin-sulbactam, Sultamicillin (combination of
ampicillin and sulbactam; has its own antibiotic property
Table 7. Pneumonia Severity Index so it has a better coverage than co-amoxiclav),
Risk Mortality % Recommended Piperacillin-tazobactam
Point total Risk Cephalosporins
Class (No. of Pts) Site of Care
No Low I 0.1(3,034) Outpatient 1st generation: no role in empiric treatment
predictors
< 70 Low II 0.6(5,778) Outpatient 2nd: Cefuroxime, Cefaclor (it is known to cause resistance
so Cefuroxime is more commonly used) ; 2nd generation
cephalosporins target gram positive organisms
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3rd: Oral or parenteral amoxicillin/ clavulanate (2 g bid); alternatives: ceftriaxone (12 g IV

- Anti-Pseudomonal: Ceftazidime, Cefoperazone qd), cefpodoxime (200 mg PO bid), cefuroxime (500 mg PO bid)] +
- Without anti-pseudomonal coverage: Ceftriaxone, Macrolide
Cefotaxime, Cefpodoxime (Cefpodoxime is similar **In regions with a high rate of high-level pneumococcal macrolide
to 2nd generation cephalosporins as far as resistance, consider alternatives listed above for patients with
antimicrobial coverage is concerned) comorbidities
4th: Cefepime, Cefpirome; their effect is concentrated Inpatients
more on gram-negative organisms including Non-ICU
Pseudomonas aeruginosa Respiratory fluoroquinolone [moxifloxacin (400 mg PO or IV qd),
In giving cephalosporins you should start from gram gemifloxacin (320 mg PO qd), levofloxacin (750 mg PO or IV qd)] or
positive to gram negative and lastly to anti-pseudomonal Beta-lactam [cefotaxime (12 g IV q8h), ceftriaxone (12 g IV qd),
coverage ampicillin (12 g IV q46h), ertapenem (1 g IV qd in selected
Carbapenems drug of choice for extended spectrum beta patients)] + Macrolide [oral clarithromycin or azithromycin (as
lactamase (ESBL)-producing organisms like klebsiella, proteus listed above for previously healthy patients) or IV azithromycin (1 g
and E.coli. once, then 500 mg qd)]
Non-anti-Pseudomonal: Ertapenem (given once a day) ICU
Anti-Pseudomonal: Imipenem (earliest), Meropenem, Beta-lactam [cefotaxime (12 g IV q8h), ceftriaxone (2 g IV qd),
Doripenem (latest and has more SE such that when it is ampicillin-sulbactam (2 g IV q8h)] + Azithromycin or a
used in sepsis, patients are more commonly dying) fluoroquinolone (as listed above for inpatients, non-ICU)
Monobactam example is aztreonam
Special Concerns
o Macrolides good for atypical organisms and also covers for
If Pseudomonas is a consideration
Streptococcus pneumoniae
Antipneumococcal, antipseudomonal Beta-lactam [piperacillin/
Erythromycin has more GI side effects like gastritis and
tazobactam (4.5 g IV q6h), cefepime (12 g IV q12h), imipenem (500
vomiting
mg IV q6h), meropenem (1 g IV q8h)] + either Ciprofloxacin (400
Clarithromycin, Dirithromycin lesser GI side effects
mg IV q12h) or Levofloxacin (750 mg IV qd) or
compared to erythromycin
Azithromycin not a true macrolide but rather an azalide; its The above Beta-lactams + an aminoglycoside [amikacin (15 mg/kg
activity is similar to macrolide; used only once a day but in qd) or tobramycin (1.7 mg/kg qd) and azithromycin] or
CAP it is given 3 times a day (tablet) The above Beta-lactams + an aminoglycoside + an
o Tetracyclines considered as newer macrolides antipneumococcal fluoroquinolone
Tetracycline can cause dental staining If CA-MRSA is a consideration
Doxycycline available in the Philippines Add linezolid (600 mg IV q12h) or vancomycin (1 g IV q12h).
Minocycline
o Fluoroquinolones Table 9. Philippine CAP Guidelines 2010
Weak anti-pneumococcal activity: Ciprofloxacin, Ofloxacin, Risk Stratification Potential Pathogens Empiric Therapy
Norfloxacin, Pefloxacin; they are good for gram-negative Low risk CAP S. pneumoniae AMOXICILLIN
organisms as they are being used for typhoid fever but their (previously H. influenzae or
activity is not good when used against Streptococcus healthy) C. pneumoniae EXTENDED MACROLIDES
pneumoniae M. pneumoniae (suspected atypical
APFQ (Antipneumococcal fluoroquinolones): Moxifloxacin M. catarrhalis pathogen)
(has good activity against tuberculosis especially for the drug- Amoxicillin is given 3 grams per day in 3 divided doses
resistant TB), Levofloxacin, Gatifloxacin, Gemifloxacin; newer Low Risk CAP S. pneumoniae BETA LACTAMASE
fluoroquinolones and they have good activity against (stable co- morbid H. influenzae INHIBITOR
Streptococcus pneumonia and atypical organisms like illness or recent C. pneumoniae COMBINATION (BLIC)*
mycoplasma and legionella; Gatifloxacin was pulled from the antibiotic therapy) M. pneumoniae OR
market because of hepatotoxicity M. catarrhalis 2ND GENERATION
o Aminoglycosides relatively cheap and has good gram-negative Enteric G(-) CEPHALOSPORIN
activity including Pseudomonas; adverse effect is ototoxicity and bacilli +/-
nephrotoxicity EXTENDED MACROLIDES
Streptomycin, Gentamycin, Tobramycin, Amikacin these Alternative:
drugs have good activity against TB 3rd generation oral
o Glycopeptides examples are vancomycin and bleomycin CEPHALOSPORIN +/-
extended MACROLIDE
Table 8. Empirical Antibiotic Teatment of Community Acquired Pneumonia Remember respiratory fluoroquinolone can replace the two
Outpatients combinations because of the better coverage and they have same
Previously healthy and no antibiotics in past 3 months bioavailability whether tablet or IV preparation as advantage
Macrolide [clarithromycin (500 mg PO bid) or azithromycin (500 mg Moderate Risk CAP S. pneumoniae IV NON-PSEUDOMONAL
PO once, then 250 mg qd)] or H. influenzae BETA LACTAM
Doxycycline (100 mg PO bid) C. pneumoniae (BLIC/CEPHALOSPORIN/
Comorbidities or antibiotics in past 3 months: select an alternative M. pneumoniae CARBAPENEM)
from a different class M. catarrhalis +
Respiratory fluoroquinolone [moxifloxacin (400 mg PO qd), Enteric G(-) EXTENDED MACROLIDE
gemifloxacin (320 mg PO qd), levofloxacin (750 mg PO qd)] or bacilli or
Beta-lactam [preferred: high-dose amoxicillin (1 g tid) or L. pneumophila IV NPBL + RESPIRATORY
Anaerobes* FQ
Group 19 | Pio, Raph, Jobs, Nica, Pao Page 7 of 11
 MEDICINE 5.1

Ertapenem is the non-pseudomonal carbapenem that can be used for HAP, VAP, HCAP
this purpose DEFINITION
IV NPBL + Respiratory fluoroquinolones are reserved as last resort HAP (Hospital-Acquired Pneumonia)
especially if resistance happens o Pneumonia that occurs 48 hours or more after hospital
High Risk CAP (no S. pneumoniae IV NPBL admission, which was not incubating at the time of admission
risk factors for P. H. influenzae (BLIC/cephalosporin/ VAP (Ventilator-Acquired Pneumonia)
aeruginosa) C. pneumoniae Carbapenem) o Pneumonia that arises 48-72 hours after endotracheal intubation
M. pneumoniae + HCAP (Health Care-Associated Pneumonia)
M. catarrhalis IV Extended Macrolide Pneumonia in any patient who was hospitalized in an acute care
Enteric gram- or hospital for 2 or more days within 90 days of infection; resided in a
negative bacilli IV Respiratory FQ nursing home or long-term facility; received recent intravenous
L. pneumophila antibiotic therapy, chemotherapy, or wound care within the past
Anaerobes* 30 days of the current infection; or attended a hospital or
hemodialysis clinic
High Risk CAP (with S. pneumoniae IV Anti-pneumococcal,
risk factors for P. H. influenzae Anti-Pseudomonal Beta RISK FACTORS FOR HCAP
aeruginosa) C. pneumoniae Lactam Hospitalization for 2 days or more in the preceding 90 days
M. pneumoniae (BLIC/Carbapenem/ Residence in a nursing home or extended-care facility
M. catarrhalis Cephalosporin) Home infusion therapy (including antibiotics)
Enteric gram- + Chronic dialysis within 30 days
negative bacilli IV extended macrolide + Home wound care
L. pneumophila IV Aminoglycoside Family member with MDR pathogen
Anaerobes* OR
P. aeruginosa IV APn, APs BL Table 11. Clinical Conditions Associated With and Likely Pathogens In Health Care-
+ Associated Pneumonia
IV ciprofloxacin/ Pathogen
levofloxacin P. Aci MDR
Risk Factor MRSA
Levofloxacin 750mg daily has also anti-pseudomonas activity aeruginosa spp. Ent
Hospitalization for 48 h
Complications Hospitalization for 2 days in prior 3
Metastatic Infection months
o Unusual Nursing home or extended-care-
o E.g. endocarditis, brain abscess facility residence
Antibiotic therapy in preceding 3
Lung abscess
months
o Those with necrotizing infections
Chronic dialysis
Complicated parapneumonic effusion
o Diagnosed by thoracentesis Home infusion therapy
o Requires drainage Home wound care

Measures for Prevention of CAP Family member with MDR infection

Smoking cessation **Aci spp.: Acinetobacter spp., MDR Ent: MDR Enteriobacteriociae,
Vaccines: Influenza and Pneumococcal
Reducing effect of comorbidities: control CHF, hyperglycemia Table 12. Empirical Antibiotic Treatment of Health CareAssociated Pneumonia
Table 10. 2012 Update of Routine Immunization for Filipino Adults Patients without Risk Factors for MDR Pathogens
Vaccine Type/ Route Target Individuals (age 50 years old) Ceftriaxone (2 g IV q24h) or
PNEUMOCOCCAL Immunocompromised Conditions Moxifloxacin (400 mg IV q24h), ciprofloxacin (400 mg IV q8h),
Polysaccharide Functional asplenia (sickle cell disease or levofloxacin (750 mg IV q24h) or
(PPSV23) IM/SC and other hemoglobinopathies, splenic Ampicillin/sulbactam (3 g IV q6h) or
Conjugate (PCV13) dysfunction) Ertapenem (1 g IV q24h)
this is the one preferred Anatomic asplenia (congenital asplenia Patients with Risk Factors for MDR Pathogens
now and not the old and splenectomy [if elective -lactam:
PPSV23 - IM splenectomy is planned, vaccinate at o Ceftazidime (2 g IV q8h) or cefepime (2 g IV q812h) or
least 2 weeks before surgery]) o Piperacillin/tazobactam (4.5 g IV q6h), imipenem (500 mg IV q6h
Generalized malignancy or 1 g IV q8h), or meropenem (1 g IV q8h) plus
Solid organ or bone marrow A second agent active against gram-negative bacterial pathogens:
transplants o Gentamicin or tobramycin (7 mg/kg IV q24h) or amikacin (20 mg/
Leukemia, Lymphoma kg IV q24h) or
Multiple myeloma o Ciprofloxacin (400 mg IV q8h) or levofloxacin (750 mg IV q24h)
Human immunodeficiency virus plus
infection An agent active against gram-positive bacterial pathogens:
Chronic renal failure or nephrotic o Linezolid (600 mg IV q12h) or
syndrome o Vancomycin (15 mg/kg, up to 1 g IV, q12h)
Receiving immunosuppressive therapy,
including corticosteroids
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 MEDICINE 5.1

ETIOLOGY OF HAP, VAP, HCAP Risk Factors for MDR Pathogens

Non-MDR Pathogens MDR Pathogens Antimicrobial therapy in the preceding 90 days (some consider up to 6
S. pneumoniae P. aeruginosa months)
Other streptococcus spp. MRSA Current hospitalization of 5 days or longer
H. Influenzae Acinetobacter spp. High frequency of antibiotic resistance in the community or specific
MSSA ATB-resistant hospital unit
ATB-sensitive Enterobacteriaceae Presence of risk factors for HCAP
Enterobacteriaceae Enterobacter spp. Immunosuppressive disease and/or therapy
E. Coli ESBL-positive strains
K. pneumoniae Klebsiella spp. Clinical Manifestations/Diagnosis
Proteus spp. Legionella spp. Lower respiratory signs/symptoms
Enterobacter spp. Bulkholderia cepacia o Cough
S. Marcescens Aspergillus spp o Rhonchi
o Wheezing
UNCOMMON CAUSES OF VAP o Purulent sputum
Legionella species Changes in lab parameters
Anaerobes o New/progressive radiodensities
Fungi o Leukocytosis or leukopenia
Viruses o Worsening of blood oxygenation
Pneumocystis jiroveci Differential diagnosis
o Pulmonary Thromboembolism
EPIDEMIOLOGY o Pulmonary Edema
Early-onset HAP/VAP o Pulmonary Hemorrhage
o Within first 4 days of hospitalization o Drug Reaction
o Better prognosis o Tracheobronchitis
o Caused by antibiotic-sensitive bacteria
Clinical Strategy
Late-onset HAP/VAP
o > 5days of hospitalization Diagnosis by new or progressive radiographic infiltrate plus at least 2 of
o Caused by multidrug-resistant (MDR) pathogens the following:
o patient mortality and morbidity o Fever >38oC
o Leukocytosis or leukopenia
CANADIAN HAP AND VAP GUIDELINES 2008: RISK FACTORS o Purulent secretions
Oropharyngeal colonization with pathogenic organisms In hospitalized patients, especially those on mechanical ventilator,
application of clinical criteria often results in overdiagnosis of
Host factors: supine positioning, extensive burns, mechanical
pneumonia
ventilation, cardiothoracic surgery, ARDS, head trauma (head trauma is
a risk factor for acquiring MRSA; also neurosurgical procedures) In an attempt to reduce the tendency of overdiagnosis, a modified CPIS
score was proposed and was first used in 1991
Environmental factors: nasogastric tubes, ventilator tubing condensate
(these can be potentially infected, and therefore, increase the risk of the
Table 13. Clinical Approach to Diagnosis of HAP/VAP
patient for developing VAP)
CPIS pts 0 1 2
Acid-suppressing drugs Chest X-ray
o Critically ill patients, especially trauma patients, have an increased None Diffuse Localized
Infiltrates
risk of upper GI bleeding; therefore, they are routinely given acid- Temperature (oC) 36.5 38.4 38.5 38.9 >39 or <36
suppressing drugs. When the pH of the GIT is altered, it gets <4,000 or >11,000
Leukocyte Count 4,000 11,000 <4,000 or >11,000
colonized by organisms that can be vomited and aspirated into the + band forms >500
respiratory tree. <240 + no
PaO2/FIO2 >240 or ARDS
evidence of ARDS
SOURCES OF MICROORGANISMS CAUSING HAP AND VAP Microbiology
(-) rare or light (+) moderate or (+) and compatible
(Tracheal
growth heavy growth with gram stain
Aspirate)
Endogenous Exogenous Progression of
Oropharynx Health care Progression, no
Chest X-ray (Day No progression
Trachea workers CHF or ARDS
3)
Nasal carriage Ventilatory If CPIS score is 6 or more, it is more likely that you are dealing with
Sinusitis Aspiration Inhalation circuits ventilator-associated pneumonia.
Gastric fluids Nebulizers Pulmonary function assessment through CPIS would indicate prognosis.
Biofilms* An increasing pulmonary function would indicate that the patient may
be on his way to recovery
Blood HAP and VAP *SEE APPENDIX FOR DIAGNOSTIC ALGORITHM BASED ON CANADIAN HAP
*Biofilms are subpopulations of microorganisms that develop inside the AND VAP GUIDELINES
endotracheal tube. Inside the endotracheal tube, biofilms are not accessible
to the antibiotic given, so when the patients secretions are suctioned, and Microbiological Approach to the Diagnosis of HAP/VAP
the suction is moved deeper into the respiratory tree, the biofilm is moved UK HAP Guidelines 2008: Respiratory Microbiological Sampling Methods
and inoculated into the lung parenchyma. Therefore patient will suffer the Endotracheal aspirate cultures
same infection from the same organism. o Not for the diagnosis of VAP
o Constantly contaminated
Group 19 | Pio, Raph, Jobs, Nica, Pao Page 9 of 11
 MEDICINE 5.1

Invasive sampling is preferred (PSB and BAL either blind or Endotracheal intubation Non-invasive ventilation
bronchoscopic) Daily awekening from sedation;
Prolonged duration of ventilation
o Same performance weaning protocols
o More likely not to be contaminated Abnormal swallowing function Early percutaneous tracheostomy
o Quantitative cultures of respiratory specimens should not be Head of bed elevated; Avoidance of
relied on for the diagnosis of HAP/VAP Secretions pooled above
reintubation; Minimize sedation;
o Quantification of intracellular organisms in BAL specimens is a endotracheal tube
Avoid supine position
rapid and specific test and can be used as a guide for therapy Tight glycemic control (but not too
To discriminate between colonization and true infection by determining Altered lower respiratory host low to avoid hypoglycemia); lowering
the bacterial burden defenses of hemoglobin transfusion threshold;
o Quantitative ETA: 106 cfu/mL specialized enteral feeding formula
o Quantitative PSB: 103 cfu/mL Prevention
o Bronchoscopic BAL: 104-105 cfu/mL o Alcohol-based hand disinfection
* PSB= Protected specimen brush; BAL= Bronchoalveolar lavage; ETA= Endotracheal o Surveillance of ICU infections
aspirate
o Avoiding or minimizing the duration of endotracheal intubation
Microbiologic Causes of VAP o Minimizing the risk of microaspiration
Non-MDR Pathogens MDR Pathogens o Preferential use of enteral nutrition
Streptococcus pneumoniae Pseudomonas aeruginosa o Use of restricted transfusion trigger policy for blood products
Other Streptococcus spp. MRSA
Haemophilus influenzae Actinobacter spp. Summary: Best Practices in HAP Management
MSSA Antibiotic-resistant Diagnostic Strategies
Enterobacteriaceae o Standardized
Antibiotic-sensitive Enterobacter spp. o Cost-effective
Enterobacteriaceae Treatment Strategies
Eschericia coli ESBL-positive strains o Appropriate/adequate initial empiric therapy
Klebsiella pneumoniae Klebsiella spp. o Local data (antibiogram)
o Minimum effective period of antibiotics
Proteus spp. Legionella pneumophila
o Do not use antibiotic if not indicated
Enterobacter spp. Burkholderia cepacia
o Immediately deescalate if with culture results
Serrata marcescens Aspergiulus spp.
Non-antibiotic therapies
Antibiotic Therapy Preventive strategies
No Risk Factors for MDR Pathogens With Risk Factors for MDR Pathogens o General infection control
Ceftriaxone Anti-pseudomonal beta-lactam o Target modifiable factors
BEST STRATEGY: Hand washing
Moxifloxacin PLUS
Levofloxacin 2nd Agent active against gram-
Ciprofloxacin negative bacteria
Ampicillin/sulbactam PLUS
3rd Agent active against gram-
Ertapenem
positive bacteria

Prevention Strategies
Pathogenic Mechanism
Oropharyngeal colonization
(ventilator)
Elimination of normal flora
Large-volume oropharyngeal
aspiration around time of
intubation
Gastroesophageal reflux
Bacterial overgrowth of stomach
Cross-infection from other
colonized patients
Large-volume aspiration
Microaspiration around
endotracheal tube
Group 19 | Pio, Raph, Jobs, Nica, Pao
Prevention Strategy
Antibiotic paste in oropharyngeal
cavity
Avoidance of prolonged antibiotic
courses (7-8 days unless its
pseudomonas then do 21 days)
Short course of prophylactic
antibiotics for comatose patients
Postpyloric enteral feeding;
avoidance of high gastric residuals;
prokinetic agents
Prophylactic agents that raise gastric
pH; selective decontamination
Hand washing, especially with
alcohol-based rub; Isolation; Proper
sterilization of equipment
Endotracheal intubation; avoidance
of sedation; decompression of small-
bowel
Page 10 of 11
 Medicine 5.1 LECTURER: Dr. Zotomayor
PNEUMONIA DATE: Jan. 06, 2015

APPENDIX

CAP RISK CLASSIFICATION AND SITE OF CARE DECISION

Two or more of the following:

o o
1. Temp. >38 C or <36 C
2. Leukoplakia or leukocytosis
3. Purulent tracheal
secretions
4. Decreased PaO2

Chest Radiographs
1. Normal NOT HAP
2. Alveolar infiltrates
3. Air bronchogram sign
4. Increasing infiltrates

Clinical Pulmonary Infection Score (CPIS)

1. Score >6: likely pneumonia
2. Score 4-6: if patient is intubated, may still consider VAP
3. Recalculated daily: may stop or dont start antibiotic therapy if <6 by
Day 3

CANADIAN HAP AND VAP GUIDELINES

Group 19 | Pio, Raph, Jobs, Nica, Pao Page 11 of 11