PULMONOLOGY, MED II - 3RD YEAR Hairs & turbinates of the

nares
Branching architecture of the
tracheobronchial tree
PNEUMONIA
(DR CONSTANTINO TRANS MIDTERMS MARCH 2017)
Gag reflex & the Normal flora
cough of
mechanisms oropharynx
WHAT IS PNEUMONIA?
 Infection of the parenchyma – alveoli, interstitium and distal airways
 Results from Microorganisms reaching the alveoli
- Proliferation of microbial pathogens at the alveolar level
- Host’s response to those pathogens
 An important cause of morbidity and mortality

?Community-Acquired Alveolar Macrophages

(assisted by local proteins

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

?Hospital-Acquired surfactant proteins A & D)
?Ventilator Associated

 Community-acquired Clear & kill pathogens

 Health-care Associated Pneumonia

- Ventilator Associated
- Hospital Acquired Mucociliary Engulf bacteria
eliminated Lymphatics
elevator
Pneumonia can be community acquired, hospital acquired and can be
ventilator associated.
CAPACITY EXCEEDED
Community Acquired Pneumonia, as the term implies, is acquired within
the community, except in the hospital setting.
INFLAMMATORY MEDIATORS
Health-care Acquired Pneumonia can be Ventilator Associated
Pneumonia or Hospital Acquired Pneumonia or it can be acquired in the Interleukin (IL-1) &
FEVER
community also. By definition when we say HEALTH-CARE ASSOCIATED tumor necrosis
PNEUMONIA (HCAP), it means it is a Pneumonia which develops within 3 factor (TNF)
months of being confined in the hospital or within 3 months of taking
antibiotics for a respiratory tract infection.
Chemokines (IL-8 and PERIPHERAL
Granulocyte colony- LEUKOCYTOSIS
HOW DO MICROORGANISMS GAIN ACCESS? stimulating factor) stimulate
Microorganisms gain access to the tracheobronchial tree by inhalation of the release of neutrophils &
contaminated droplets. This is actually the 2nd most common mode. The their attraction to the lung & INC. PURULENT
SECRETIONS
most common mode of acquiring Pneumonia is aspiration from the
oropharynx. Normally we aspirate small amounts of oral secretions during
swallowing. However in individuals who have problems of swallowing like Inflammatory mediators
those who had strokes, seizures, or who consumed a lot of alcohol, then from AM and neutrophils
they aspirate large volumes of secretions which is contaminated. You can HEMOPTYSIS
create an alveolar capillary
have Pneumonia by hematogenous spread from distant sites of infection. leak → RBCs can cross the
And then, you have contious extension from infected space or adjacent alveolar capillary membrane
infection.
 Inhaled as contaminated droplets
The capillary leak results in a HYPOXEMIA RESULTS
 Aspiration from the oropharynx FROM ALVEOLAR FILLING
radiographic infiltrate & rales
 Hematogenous spread
detectable on auscultation
 Contiguous extension from an infected pleural or mediastinal space.

Pneumonia develops by overcoming the host’s defenses. So what are the Some bacterial pathogens may
host’s defenses? We have talked about this previously. Gag reflex, cough interfere with the hypoxemic
SEVERE HYPOXEMIA
mechanism, hairs and turbinates of the nares, branching architecture of the vasoconstriction normally
tracheobronchial tree & the normal flora of the oropharynx which inhibits occurring with fluid-filled alveoli
colonization by pathogenic bacteria. So you have microorganisms
reaching in the alveoli mostly by aspiration or inhalation route. The alveolar
Increased respiratory drive in the LEADS TO
macrophages try to clear and kill the pathogens so bacteria are usually systemic inflammatory response RESPIRATORY
eliminated and are removed by mucociliary mechanism or through the syndrome (SIR) ALKALOSIS
lymphatics. However, when the capacity of the macrophages to engulf
the bacteria are exceeded, that is the time when you have Pneumonia.
 The alveolar macrophages initiate the inflammatory response to Decreased compliance due to
bolster lower respiratory tract defenses. So the inflammatory response - Capillary leak or increase
is a defense mechanism. stiffness in lung Lead to DYSPNEA
 The host inflammatory response triggers the clinical syndrome of - Hypoxemia
- Increased respiratory drive
Pneumonia. Because that will consist of producing inflammatory cells - Increased secretions
and inflammatory inhibitors that would cause inflammation on the - Occ. infection-related
parts of the lungs and that would clinically present as Pneumonia, bronchospasm
where you will find consolidation or secretions filling up the alveoli, the
symptoms that would differ because of the production of pyrogens,
If severe enough
and then you have productive cough. - The changes in lung mechanics May cause DEATH
2˚ to reductions in lung volume
and compliance
- The intrapulmonary shunting of
blood

Page 1 of 6
 PATHOLOGIC CHANGES IN PNEUMONIA BACTERIAL PATHOGENS
PHASES OF PATHOLOGIC CHANGES (LOBAR PNEUMONIA) TYPICAL ATYPICAL
You have several phases of Pneumonia. You are - S. pneumoniae - Mycoplasma pneumoniae
dealing here with Lobar Pneumonia. The initial stage Haemophilus influenzae Chlamydia pneumonia (in
EDEMA - -
should be Edema, then Red Hepatization Phase, Gray - S. aureus OP’s)
Hepatization Phase, and lastly Resolution. - Gram-negative bacilli - Legionella spp (in inpatients)
 During the 1st Phase (Edema): Presence of a  K. pneumonia - Respiratory viruses 16% of
RED proteinaceous exudate and often of bacteria  P. aeruginosa hosp. admissions
HEPATIZATION in the alveoli.  Influenza viruses
 In the Red Hepatization Phase: Presence of  Adenoviruses
erythrocytes in the cellular intraalveolar  Respiratory syncytial
GRAY exudate and viruses
HEPATIZATION  Bacteria are occasionally seen. So you have These are the examples of typical and atypical bacterial pathogens. The
the removal of bacteria during the Red main difference between the 2 would be the clinical presentation.
Hepatization Phase. Bacteria in Edema Phase

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

and more of erythrocytes in Red Hepatization In the typical type of Pneumonia, you have sudden onset of symptoms.
RESOLUTION Phase. You have fever, productive cough, pleuritic pain.
 In Gray Hepatization Phase: Predominant cells –
neutrophils, abundant fibrin deposition, and In atypical type of Pneumonia, you have insidious onset of symptoms and
bacteria have disappeared; corresponds with a lot of extrapulmonary symptoms. For example, in Mycoplasma, besides
successful containment of the infection & the Pneumonia, you can develop transverse ileitis, bullous myringitis or
improvement in gas exchange. jaundice.
 In Resolution Phase: The macrophage
reappears as the dominant cell type in the Factors which suggest the possible cause of CAP:
alveolar space, and the debris of neutrophils, FACTORS POSSIBLE PATHOGEN(s)
bacteria, & fibrin has been cleared, as has the
ALCOHOLISM S. pneumoniae,
inflammatory response. In the Gray
oral anaerobes,
Hepatization Phase, you have the neutrophils.
K. pneumonia,
In Resolution Phase, the macrophages.
Acinetobacter spp.,
Again, in Edema Phase, you have bacteria.
M. tuberculosis
In Red Hepatization: erythrocytes kaya siya red.
COPD &/or SMOKING H. influenzae,
Gray Hepatization: Neutrophil predominance.
Ps. Aeruginosa,
Resolution Phase: Macrophages.
Legionella spp.,
PATTERNS OF PNEUMONIA:
S. pneumoniae,
1. LOBAR – Pneumonia of lobar segments. In here, you can see
M. catarrhalis,
the air bronchogram. This is a homogenous density wherein you
C. pneumoniae
can see lucencies within the area of the Pneumonia.
STRUCTURAL LUNG DISEASE P. aeruginosa,
2. INTERSTITIAL – Lacey or reticular pattern of infiltrates. This is often
(e.g, Bronchiectasis)¸ Burkholderia cepacia,
seen in viral and atypical Pneumonias. Actually in Pneumocystis
commonly you have S. aureus
jiroveci Pneumonia, we have a combination of the miliary and
colonization of
interstitial patterns of Pneumonia.
Pseudomonas
3. BRONCHOPNEUMONIA – Bronchopneumonia pattern which
corresponds to the bronchial segment affected. As you can DEMENTIA, STROKE, DEC. Oral anaerobes,
see, you have filling up of the segments also. LEVEL OF CONSCIOUSNESS Gram negative enteric bacteria
4. MILIARY – Often seen in hematogenous types of Pneumonia like like seizure episodes
the initial phase of Staphylococcal infection or disseminated TB. because of the risk of
You have small nodular infiltrates all throughout the lung. aspiration.
Hematogenous spread that’s why it involves both sides of the LUNG ABSCESS, you have CA-MRSA,
lung. necrotizing organisms Oral anaerobes,
Endemic fungi,
COMMUNITY ACQUIRED PNEUMONIA M. tuberculosis,
ETIOLOGY Atypical mycobacteria
1. BACTERIA
TRAVEL, history of travel to Histoplasma capsulatum,
2. FUNGI
endemic areas Hantavirus,
3. VIRUSES
Coccidioides spp.,
4. PROTOZOA
Burkholderia pseudomallei,
But there are also other organisms:
Avian influenza virus
NEW ORGANISMS:
STAY where there are a lot Legionella spp
- HANTAVIRUSES, METAPNEUMOVIRUSES, CORONAVIRUSES, CA-MRSA
of people like IN HOTEL OR
(Methicillin resistant Staph aureus, now an emerging problem)
ON CRUISE SHIP IN
PREVIOUS 2 WEEKS
These are the possible organisms present in outpatients and hospitalized
LOCAL INFLUENZA ACTIVITY Influenza virus,
patients. In hospital patients, you divide them to Non-ICU & ICU patients.
S. pneumonia,
HOSPITALIZED PATIENTS
S. aureus
OUTPATIENTS NON-ICU PATIENTS ICU PATIENTS
EXPOSURE TO BATS OR H. capsulatum,
 Streptococcus  Streptococcus  Streptococcus
BIRDS, RABBITS, SHEEP, Chlamydia psittaci,
pneumonia pneumonia pneumonia
GOATS, PARTURIENT CATS. Francisella tularensis,
 Mycoplasma  Mycoplasma  Staphylococcus
These are not so common Coxiella burmetti
pneumonia pneumonia aureus
in Philippines but I think a
 Haemophilus  Chlamydia  Legionella spp
lot of them have been
influenza pneumonia  Gram-negative
underdiagnosed.
 Chlamydia  Haemophilus bacilli
pneumonia influenzae  Haemophilus
 Respiratory  Legionella spp infleunzae
viruses  Respiratory
viruses

Page 2 of 6
So the ff are the risk of factors depending on the type of Pneumonia. From  Bronchiolitis obliterans and organizing pneumonia
what is notable here, if you have These conditions also present with dyspnea. Some present with fever,
RISK FACTORS hemoptysis and in PE, they may have crackles. That is the reason why you
CAP, you have Alcoholism, asthma, immunosuppression, should always complete your physical examination.
comorbidities like → institutionalization, and an age of > 70 years
versus 60-69 years DIAGNOSIS OF PNEUMONIA
Pneumococcal Dementia, seizure disorders, heart failure,
pneumonia cerebrovascular disease, alcoholism, tobacco
IS THIS PNEUMONIA?
smoking, chronic obstructive pulmonary
disease (COPD), and HIV infection
CA-MRSA Skin colonization or infection with CA-MRSA
Pneumonia
Enterobacteriaceae, Recent hospitalization and/or received
CLINICAL & RADIOGRAPHIC
usually associated antibiotic therapy or who have comorbidities
with HCAP such as alcoholism, heart failure, or renal

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

failure IF SO, WHAT IS THE LIKELY ETIOLOGY?
P. aeruginosa Severe structural lung disease, such as
Bronchiectasis, Cystic Fibrosis, or Severe COPD
Legionella infection, Diabetes, Hematologic malignancy, Cancer,
affect those who Severe renal disease, HIV infection, Smoking,
have comorbidities Male gender, and a recent hotel stay or ship
also at mahilig sila cruise LABORATORY TECHNIQUES
sa crowded places
Diagnosis of Pneumonia is made by clinical and radiographic findings and
CLINICAL MANIFESTATIONS if you want to determine the etiology, you do the ff laboratory techniques.
 Fever with tachycardia CLINICAL
 Cough – may be productive or non productive  HISTORY – Risk factors, comorbid conditions – very important!
 Pleuritic chest pain – because of pleural involvement  PHYSICAL EXAMINATION – complete PE
 Fatigue, headache, myalgias, and arthralgias - most commonly in RADIOLOGIC
atypical pneumonia  CHEST XRAY
 Chills and/or sweats  CT SCAN – Sometimes you need to get a CT scan especially if
 Shortness of breath – due to pain or alveolar filling you are thinking about obstructive Pneumonia. This may be
 Hemoptysis due to the presence of a mass.
 GI symptoms: nausea, vomiting, and/or diarrhea – most commonly in
atypical pneumonia
In elderly patients, actually it is common in elderly or those with chronic
diseases, like Chronic Liver Disease or Kidney Disease, they may not have
fever, but they may develop the extrapulmonary manifestations or
changes in sensory.

PHYSICAL EXAMINATION FINDINGS

- Vary with the degree of pulmonary consolidation and the significant
pleural effusion. As usual, you follow the basic rules of chest PE. Be
systematic with Inspection, Palpation, Percussion and Auscultation
which you usually do not do when you are in QCGH.
 INSPECTION
- Inc. RR & use of accessory muscles
 PALPATION
o Inc. or dec. tactile fremitus
 PERCUSSION
o Dull to flat, reflecting underlying consolidated lung and In your upper left, you have more of a TB with lung cavitations. The same is
pleural fluid true with your Lobar type. In your upper right, you have your Pneumonia.
 AUSCULTATION In the CT scan, you have your Pneumonia with a cavitary formation.
o Crackles, bronchial breath sounds, and possibly a pleural
friction rub ETIOLOGIC DIAGNOSIS
What would be your vocal and tactile fremitus findings in Pneumonia?  Gram’s Stain and Culture of Sputum – very very important! How do you
Increased. Now if you do not have that, what do you do? What is your next get an adequate specimen? What determines the adequacy of your
maneuver? Meron kang crackles tapos wala kang increased vocal/ tactile sputum specimen? Pag saliva, ano? How do you know if it is saliva or
fremitus so you are not sure if that is Bronchiectasis, Pnuemonia or other contaminated by saliva? Diba epithelial cells! How many epithelial
disease? What is your next step? You perform your whispered pectoriloquy cells for you to say that it is saliva or contaminated saliva? Pus cells.
diba. It is a sign of early consolidation. Sometimes things can get And you have to correlate your blood stains with your cultures kasi
complicated, you may not hear the crackles or you may not feel the mamaya ang cultures ninyo Staph aureus tapos ang stain niyo gram
increase in tactile fremitus, because of ***effusion. negative bacilli. So ano yung paniniwalaan niyo? Baka mamaya
- Severely ill patients may have septic shock and evidence of organ yung Staph aureus galling sa iba. I think in that case, it is better to
failure believe your gram stain.
So you should differentiate it from other lung conditions which may have  Blood Cultures – the problem with blood cultures is it is only positive in
crackles also such as: 5-14% of cultures in blood (+). Some have questioned the use of blood
 Pulmonary edema cultures because of its very low yield. Some organisms are just
 Pulmonary infection fastidious and sometimes because of the use of antibiotics, they don’t
 Acute respiratory distress syndrome (ARDS) grow anymore. Sometimes for blood cultures, you need to request for
 Pulmonary hemorrhage an antibiotic removal device (ARD).
 Lung cancer/ metastatic cancer  Antigen Tests – Pneumococcal and certain Legionella antigens in
 Atelectasis urine
 Radiation pneumonitis  Polymerase Chain Reaction – decrease the time for the organisms to
 Drug reactions involving the lung be identified. Legionella spp., M. pneumoniae, and C. pneumonia
 Extrinsic allergic alveolitis  Serology – atypical pathogen as Coxiella burnetti
 Pulmonary vasculitis
 Pulmonary eosinophilia

Page 3 of 6
So for the TREATMENT of Pneumonia, it is based on category or degree of
severity. So Pneumonia according to the Site of Care:
SITE OF CARE
There are currently 2 sets of criteria: currently on use because they are
simple
1. Pneumonia Severity Index (PSI) – a prognostic model used to
identify patients at low risk of dying. So for risk of dying, you use
your PSI.
2. CURB-65 criteria – a severity-of-illness score
PSI – Pneumonia Severity Index
 Points given for 20 variables, age, coexisting illness, and abnormal
physical and laboratory findings
 On the basis of the resulting score, patients are assigned to one of 5
classes with the following mortality rates: Class 5 has a very high
 All criteria under moderate risk plus impending or frank respiratory
failure
- Hypoxemia with PaO2 < 60 mmHg
- Acute hypercapnia with PaCO2 > 50 mmHg
 Hemodynamic alterations and hypoperfusion:
- SBP < 90 mmHg, DBP < 60 mmHg
- Urine output < 30 cc/hr
- Altered mental state
If may patient ka in CURB-65 tapos BP, RR tapos more than 2 ang score (3-
5 ang score), high risk then they should be admitted at the ICU. For low
risk, OPD, moderate risk admission, high risk ICU.

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

chance of dying
o Class 1 – 0.1%
o Class 2 – 0.6%
o Class 3 – 2.8%
o Class 4 – 8.2 %
o Class 5 – 29.2%
 Routine use of the PSI results in lower admission rates for class 1 and
class 2 patients
 In classes 4 & 5 – patients should be admitted to the hospital;
 Class 3 – be admitted to an observational unit until a further decision
can be made
CURB-65
The CURB-65 criteria include 5 variables:
Confusion (C); with the presence of sensorial changes
Urea >7 mmol/L (U);
Respiratory rate equal to or greater than 30/min (R);
Blood pressure, systolic less than or equal to 90 mmHg or diastolic 60
mmHg (B)
Age 65 years (65)
They are assigned 1 point each.
 Patients with a score of 0, among whom, for example you have a 20
year old male without tachypnea, no increase in urea, normal BP,
the 30-day mortality rate = 1.5%, can be treated outside the hospital
or OPD basis.
 With a score of 2, the 30-day mortality rate is 9.2%, and patients
should be admitted to the hospital.
 Among patients with scores of 3, mortality rates are 22% overall;
patients may require admission to an ICU. CASE SCENARIO 1
This is much simpler and can be used at the ER for determining what you  A 25 year old Pharmacist, nonsmoker
should do to a patient with Pneumonia.  Cough and colds, 10 days PTA, after soaked in rainwater, took PPA
tabs
RISK FOR CATEGORIES FOR CAP  2 days PTA, fever & chills, cough and more severe
 Low risk CAP  Phlegm noted to be yellowish
 Moderate risk CAP  Mild chest pain on the right
 High risk CAP  VS: BP = 110/70 mmHg, RR = 23 cpm, CR= 95/min, T= 38 C
This was developed because not only the risk was identified, but also  Chest lungs – minimal crackles on the right lower lung fields
whether the patient should be admitted and the antibiotic treatment that Anong CAP ito? Low or moderate type? Then, apply the CURB-65.
should be given.
EMPIRICAL ANTIBIOTIC TREATMENT
LOW RISK CAP LOW RISK CAP: EMPIRICAL ANTIBIOTIC TREATMENT
 Stable vital signs This is a textbook treatment but currently we have guidelines based on the
RR < 30/min infectious diseases recommended by the American Thoracic Society and
PR < 125/min Infectious Diseases Society of America.
SBP >90, DBP >60 mmHg  Previously healthy and no antibiotics in past 3 months
Temp < 40 C - MACROLIDE
 No stable co-morbid conditions Clarithromycin 500 mg BID
- DM, neoplastic disease, neurologic disease, CHF Class 1, CAD, Azithromycin 500 mg OD or
Immunosuppresive therapy Doxycycline 100 mg BID
 Comorbidities or antibiotics in past 3 months: select an alternative
MODERATE RISK CAP - RESPIRATORY FLUOROQUINOLONE
 Abnormal Vital signs: any RR > 30/min, PR > 125/min, Temp >40 C Moxifloxacin 400 mg OD
 X-ray findings of Gemifloxacin 320 mg OD
- Multi-lobar involvement Levofloxacin 750 mg OD or
- Progression of lesion to 50% within 24 hours - A ß-LACTAM
- Abscess Preferred: High-dose Amoxicillin (1 g TID) or
- Pleural effusion Amoxicillin/Clavulanate 2 g BID
- Suspected Aspiration with pulmonary findings of sepsis, Alternatives:
hematologic or endocrine abnormalities Ceftriaxone 1-2 g IV QD
 Unstable comorbid condition: uncontrolled DM, active malignancies, Cefpodoxime 200 mg PO BID
neurologic disease in evolution, CHF Class II-IV, unstable CAD, Cefuroxime 500 mg PO BID
unstable angina, renal failure on dialysis, uncompensated COPD, Plus
decompensated liver disease a Macrolide

HIGH RISK CAP CASE 2

Page 4 of 6
 62 years old, Male, previous smoker, driver
 3 years history of COPD, on maintenance – LABA & LAMA
 2 weeks PTA, nonproductive cough – no meds taken
 1 week PTA, productive or whitish phlegm
- mild dyspnea, took mucolytic agent
 1 day PTA, dyspnea progressed, left sided chest pain, fever, low
grade
 BP = 110/70 mmHg, RR=28/min, CAR = 95/min, T = 38.5 C
 Chest and lungs – wheezes on both lung fields, crackles on left mid-
lung field
Bakit MODERATE? Left lang yung crackles e. Yung wheezes both lungs. So
bakit siya moderate? Sino ang low risk at moderate risk? Paano mo nasabi
na multilobar? Wala naman CXR! So may comorbidity diba, meron or
wala? Meron, may COPD. Stable or unstable morbidity? Unstable, may
exacerbations may wheezes e! Nag progress pa nga ang dyspnea. So

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

moderate risk iyan.

MODERATE RISK CAP (INPATIENT: NON-ICU): EMPIRICAL ANTIBIOTIC

TREATMENT
 A Respiratory FLUOROQUINOLONE
Moxifloxacin 400 mg PO qd
Gemifloxacin 320 mg PO qd
Levofloxacin 750 mg PO qd or
 A B-LACTAM
Ceftriaxone 1-2 g IV qd
Ampicillin 1-2 g IV q4-q6h
Cefotaxime 1-2 g IV q8h
Ertapenem 1g IV qd, plus
a MACROLIDE
Oral Clarithryomycin 500 mg PO bid
Azithromycin 500 mg PO once, then 250 mg qd
or IV AZITHROMYCIN 1 g once, then 500 mg qd

CASE 3
 80 year old, female, non smoker
 History of mild stroke 3 years ago, known
 Because weak, bedridden for the past year
 1 week PTA, noted to be anorexic, weaker
 Occasional dry cough, no fever, sleeping most of the time
 BP = 80/50, CAR = 120/min,
 Less responsive crackles noted on both lower lung fields
Ito yung sinasabi ko sometimes they do not present with symptoms of
Pneumonia, like fever, productive cough. So like this one, weak, anorexic
tapos tulog lang. Then you’ll discover crackles. GENERAL CONDITIONS
 Adequate hydration
Bakit moderate? Bakit high risk? Unstable vital signs, age. So HIGH RISK. But  Oxygen therapy for hypoxemia
there is no risk for Pseudomonas for this case kasi wala siyang prior history  Assisted ventilation when necessary
ng intake of antibiotics and does not stay in a nursing home.
FAILURE TO IMPROVE WITHIN 48-72 HRS FF. THERAPY
HIGH RISK CAP (NO RISK FOR PSEUDOMONAS): EMPIRICAL ANTIBIOTIC  Noninfectious condition
TREATMENT - Cancer, embolus, hemorrhage
 A BETA LACTAM  Resistant pathogen
Cefototaxime 1-2 gm IV q8h  Wrong drug
Ceftriaxone 2gm IV OD So you have 3rd gen cephalosporins or  Right drug, wrong dose
you can use  Unusual pathogens
Ampicillin-Sulbactam 2 gm IV q8 - Mycobacterial, anaerobic, viral, fungal
Plus Azithromycin or a Fluoroquinolone  Nosocomial superinfections especially if they worsen 72 hours after
therapy
SPECIAL CONCERNS: EMPIRICAL ANTIBIOTIC TREATMENT
 If Pseudomonas is a consideration COMPLICATIONS OF CAP
- PIPERACILLIN/TAZOBACTAM 4-5 gm IV q4-q6, CEFEPIME 1-2 gm IV  Respiratory failure – the most common
q12, IMIPINEM 500 mg IV q6, MEROPENEM 1 g IV q8.  Shock, Multiorgan failure – from sepsis
 Bleeding diathesis
+ either CIPROFLOXACIN 400 mg IVq12 or LEVOFLOXACIN 750 mg IV OD  Exacerbation of comorbid illnesses
 Metastatic infections
 Brain abscess, Endocarditis
- The above beta lactams + aminoglycoside (AMIKACIN 15 mg/kg OD
 Lung abscess – usually occurs in the setting of aspiration – should be
or TOBRAMYCIN 1.7 mg/kg/OD) + AZITHRYMYCIN drained
- The above beta lactams + aminoglycoside + antipneumococcal  Pleural effusion – should be tapped for diagnostic and therapeutic
fluoroquinolone purposes

 If CA-MRSA is a consideration is a consideration RULE OF RESOLUTION OF PHYSICAL AND LABORATORY ABNORMALITIES

- Add LINEZOLID 600 mg IV q12 or VANCOMYCIN 10 mg IV ABNORMALITIES DURATION
Fever 2-4 days
Cough 4-9 days
Crackles 3-6 days
Leukocytosis 3-4 days
C-reactive protein 1-3 days
CXR abnormalities 4-12 weeks

Page 5 of 6
Patient is considered to have responded if  Worsening oxygenation
1. Fever declines within 7 hrs  Increased minute ventilation
2. Temperature normalizes within 72 hrs Actually in the PSI or Pneumonia Severity Index, the most sensitive indicator
3. Respiratory signs (tachypnea) return to normal of improvement or worsening would be the oxygen requirement of the
patient. If your O2 requirement is decreasing, then the patient is improving.
RISK CATEGORIES OF CAP & ITS ASSOCIATED MORTALITY RATE If the O2 requirement is increasing, then the patient is worsening.
Low Risk <5%
Moderate Risk 21% EMPIRICAL ANTIBIOTIC TREATMENT OF HCAP
High risk 36% - almost high, practically 1/3  WITHOUT RISK FACTORS FOR MDR PATHOGENS
- CEFTRIAXONE 2 g IV q24 hours or
IMMUNIZATION - MOXIFLACIN 400 mg IV q8 hours
PNEUMOCOCCAL VACCINE INFLUENZA VACCINE o Ciprofloxacin 400 mg IV q8 hours
> 60 years old > 50 years old o Levofloxacin 750 mg IV q24 hours
Chronic Illness: Chronic Illness - AMPICILLIN/SULBACTAM 3 mg IV q6 hours or
CVD, Lung Disease, Immune Sx Disorder - ERTAPENEM 1 gm IV q24 hours

CAYRAPF – MED II, PULMONOLOGY - FEBRUARY 2017, 2ND SEMESTER

DM, Alcohol Abuse, Residents of Nursing Homes  PATIENTS WITH RISK FACTORS FOR MDR PATHOGENS
Chronic Liver Disease, Health Care Workers 1. A beta-lactam
Asplenia Persons in contact w/ high risk Ceftazidime 2 gm IV q8 hours or
Immune System Disorder patients Ceftapime 2 gm IV q8-q12 hours or
HIV, malignancy Piperacillin/Tazobactam 4.5 gm IV q6 hours,
Given every 5 years Given yearly Imipenem 500 mg IV q6 hours or 1 gm IV q8 hours,
Meropenem 1 gm IV q8 hours plus
HEALTH CARE-ASSOCIATED PNEUMONIA (HCAP) 2. A 2nd agent active against G (-) bacterial pathogens
 Hospitalization for 2 or more days within 90 days of the present Gentamicin or Tobramycin 7 mg/kg IV q24 hours or
infection or 3 months Amikacin 20 mg/kg IV q24 hours or
 Resident of a nursing home or long-term care facility
Levofloxacin 750 mg IV q24 hours plus
 Received recent IV antibiotic therapy, chemotherapy or wound care
3. An agent active against G(+) bacterial pathogens
in the past 30 days of the current infection
Linezolid 600 mg IV q24 hours or
 Attended a hospital or hemodialysis clinic
Vancomycin 15 mg/kg IV q12 hours. These are usually given
The reason why this has been separated from a different category is
for Staph aureus.
because the organisms involved are similar to Hospital Acquired
Pneumonia. They are treated differently from CAP, even if they were
COMPLICATIONS
acquired in the community, the management is somewhat different.
 Death
 Prolonged mechanical ventilation
DEFINITIONS:
 Prolonged hospital stay
VENTILATOR ASSOCIATED PNEUMONIA (VAP)
 Development of necrotizing Pneumonia
 Pneumonia that arises more than 48-72 hours after endotracheal
 Long-term pulmonary complications like Bronchiectasis
intubation
 Inability of the patient to return to independent functioning
HOSPITAL ACQUIRED PNEUMONIA (HAP)
 Pneumonia that occurs 48 hours or more after admission which was
PROGNOSIS
not incubating at the time of admission. So they were treated for
 HCAP is associated with significant mortality (50-70%) Why? Because
something else, but after 48-72 hours of admission, they developed
it usually involves elderly patients and they usually consists of MDR
Pneumonia. They were not intubated kasi kung intubated that would
pathogens.
be VAP.
 Presence of underlying diseases increases mortality rate
 Causative pathogen also plays major role
MICROBIOLOGICAL CAUSES OF VAP
NON-MDR PATHOGENS MDR PATHOGENS
COMPLICATION OF VAP
Strep. pneumonia P. aeruginosa
 Mortality or death
Other Streptocococus spp MRSA
 Prolong mechanical ventilator use
H. influenza Acitenobacter spp
 Pulmonary hemorrhage
MSSA Antibiotic-resistant Enterobac-
 Bronchiectasis
Antibiotic-sensitive Enterobacteriaceae teriaceae
 Parenychmal scarring
Escherichia coli ESBL-positive strains
 Muscle loss & general debilitation
Klebsiella pneumonia Klebsiella spp
Proteus spp Legionella pneumophilia
PREVENTION
Enterobacter spp Burkholeria cepacia
 Decreasing likelihood of encountering the pathogen
Serratia marcescens Aspergillus
o Hand washing – very important
Usually if you have an early onset of VAP, you have the NON-MDR
o Use of gloves and face mask
pathogens, so within 6 days. If the Pneumonia develops 6 days after being
o Negative pressure room
placed in a respirator, you have a late-onset VAP, and you have more of a
o Prompt institution of effective chemotherapy for patients
MDR pathogens.
with contagious disease
o Correction of condition that facilitate aspiration
PATHOGENESIS OF VAP
o Maintenance of gastric acidity
 Pathogenesis of the oropharynx with pathogenic microorganisms
 Strengthening the host’s response once the pathogen is encountered
 Aspiration from the oropharynx into the lower resp. tract through the
o Chemoprophylaxis
surrounding cuff of the Endotracheal Tube
o Immunizing of patients at risk
 Compromise of the normal host defense mechanisms because of the
presence of the Endotracheal Tube.

CLINICAL MANIFESTATION -LIGHT-

 Fever
Please do not rely on this. Double check for any mistakes. Read
 Leukocytosis
 Increase in respiratory secretions
the book and study well. God bless, doctors! Thank you.
 PE findings of consolidation CAyraPF
 New or changing radiographic infiltrate
 Tachypnea
 Tachycardia
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