COMMUNITY ACQUIRED

PNEUMONIA

ANG GOBONSENG, ED GERARD R.

MEDCLERK
 CASE

General data: This is a case of Q.D., 86, F,

CC: Fever and chills

Reliability of 85%

Informant is the Patient herself

 CASE

HPI:
 5 days PTA patient had onset of productive cough
characterized with whitish sputum discharge, no hemoptysis,
no fever, no chills, no medications taken and patient tolerated
her condition.
 2 days PTA patient had onset of undocumented high fever,
with persistence of symptoms, no hemoptysis noted. Patient
took 1 dose of Paracetamol 500 which gave slight relief.
 PM PTA patient still had persistence of symptoms hence
consult.
 CASE

PMH
 Patient has been hypertensive for 20 years, non diabetic, no history of bronchial
asthma, no malignancies. Patient had been hospitalized in 2010 for similar
symptoms but cannot recall the diagnosis of the physician at that time. Patient
had cholecystectomy in 1980’s. Patient is taking Amlodipine 5mg OD.
FH
 Both maternal and paternal sides are hypertensive. Patients mother had breast CA
P&SH
 Non alcoholic, non smoker, patients current occupation is a housewife.
OBH
 G6P4(3304)
 Menopause 50+
 No complications at birth, no caesarean, and gave birth through traditional
healers.
 CASE

ROS
 Large ruptured mass on left side of face
 White halo around the eyes
 Multiple teeth loss and oral cavities
 Slight dark discoloration on ankles
 CASE

PE
 General: Awake, alert, concious , coherent, not in respiratory distress
 V/S: T:38 PR:104 RR:28 BP: 130/70 O2: 96% RBS: 169
 Skin: Senile turgor, no pallor , no cyanosis
 HEENT: normocephalic, pale palpebral conjunctiva, anicteric sclera,
moist lips and oral mucosa
 Neck: supple, no LAD, no tracheal deviation, no mass
 Chest: equal chest expansion, bibasilar crackles
 CVS: Adynamic pericordium, PMI at 5th ICS, distinct heart sounds, no
murmurs
 Abdomen: Flabby, normoactive bowel sounds, tympanitic, non tender
 GUT: (-)KPS
 EXT: good ROM, strong peripheral pulses
 CASE

Neurologic:
 Oriented to time, place, person
 Cranial Nerves:
 I – not tested
 II – intact visual fields
 III,IV,VI – intact EOM
 V – intact corneal reflex
 VII – symmetric face, can smile
 VIII – intact hearing
 IX,X – intact gag reflex
 XI – symmetrical shoulder shrugg
 XII – no tongue deviation
 ON ADMISSION

Diet : Full, low cholesterol diet

IVF: PNSS 1L at 33gtts/min
Labs :
 CBC , Na, K, Crea, BUN, RBS, now then q6hr INITIAL IMPRESSION
 ABG, FBS, Lipid profile, Trop T CAP-MR
 Chest Xray PA, 12 lead ECG, U/A
Medications:
 Ceftriaxone (ODICEF) 2g IV OD
 Azithromycin (ZENITH) 500mg/tab 1 tab OD
 N- Acetylcyteine (EXFLEM) 600mg/sachet 1 sachet in ½ glass water OD
 Hydrocortisone 100mg IV q8h
 Salbutamol neb 1 neb q8h
 Felodipine 500mg/tab 1tab OD
Monitor V/S q4h
I And O q shift
Paracetamol 500mg / tab 1 tab T>=38C
 1st HOSPITAL DAY

Referral to physician for L cheek nodule once w/

consent.
Chest X Ray
result
Chest X Ray
result
LABORATORY
LABORATORY
LABORATORY
LABORATORY
 2nd HOSPITAL DAY

Given Glictazide (DIAMICRON) 60mg/tab 1 tab OD

prior to breakfast.
Reduce RBS monitoring to BID (5am – 5pm)
IV PNSS 1L at 33gtts/min
 3rd HOSPITAL DAY

Reduce Hydrocortisone 100mg 1 IV

Provide Medical certificate and abstract.
Adjunctive 7 day course of low dose hydrocortisone
IV in patients with CAP hastens clinical recovery and
prevents the development of sepsis-related
complications with a significant reduction in the
duration of mechanical ventilation, duration of IV
antibiotics and length of hospital stay with the
improvement in hospital outcome and weaning
success from mechanical ventilation.
DISCUSSION
 DEFINITION
Pneumonia
 infection of the pulmonary parenchyma
 results from the proliferation of microbial pathogens at the
alveolar level and the host’s response to those pathogens.
1. Community acquired pneumonia
2. Hospital acquired pneumonia
3. Ventilator associated pneumonia
 Colonization of the oropharynx with pathogenic
microorganisms
 Aspiration of organisms from the oropharynx into the lower
respiratory tract
 Compromise of normal host defense mechanisms
Health Care associated pneumonia
 PATHOPHYSIOLOGY

• “Proliferation of microbial pathogens at the alveolar level and

the host’s response to those pathogens.”
• Microorganisms gain access lower respiratory tract:
 Aspiration form the orophaynx
 Inhaled as contaminated droplets
 Hematogenous spread
 Contigous extension infected pleura or mediastinal space
 PATHOPHYSIOLOGY

Mechanical Alveolar
Factors level
• Hairs and tribunates
• Macrophages
• Branching
• Epithelial cell
tracheobronshial tree
surfactants A&D
• Gag reflex and cough
• Normal flora of the
oropharynx

The host inflammatory response, rather than

proliferation of microorganisms, triggers the clinical
syndrome of pneumonia.
 PATHOPHYSIOLOGY

Host inflammatory response

 Interleukin 1 and tumor necrosis factor
 fever
 Interleukin 8 and granulocyte colony
 release of neutrophils
WE CAN EXPECT THE FF:
1. Capillary leak
2. Increased respiratory drive
 PATHOPHYSIOLOGY

1. Capillary leak results in:

1. Hemoptysis
2. Radiologic infiltrates on CXR
3. Rales on auscultation
4. Hypoxemia
Alveolar filling Bacteria that interfere with
hypoxemic vasoconstriction

Severe Hypoxemia
 PATHOPHYSIOLOGY

2. Increased respiratory drive

CO2 expenditure

Respiratory alkalosis

Important to note that if symptoms are sever enough

eventually lead to VQ mismatch which will be the
cause of patient death
 PATHOLOGY (4 PHASES)

1. Edema
2. Red hepatization
3. Gray hepatization
4. Resolution
This pattern has been described best for lobar
pneumococcal pneumonia and may not apply to
pneumonia of all etiologies.
 Edema Phase

• Proteinaceous exudate
• bacteria in alveoli
 Red hepatization

• Presence of RBC in the cellular intraalveolar exudate

• Bacteria occasionally seen in specimens collected at this time
 Gray hepatization

1. no new erythrocytes are extravasating, and those

already present have been lysed and degraded.
2. The neutrophil is the predominant cell
3. Fibrin deposition is abundant
4. Bacteria have disappeared.
This phase corresponds with successful containment
of the infection and improvement in gas exchange.
 Resolution

the macrophage reappears as the dominant cell type

in the alveolar space
the debris of neutrophils, bacteria, and fibrin has
been cleared, as has the inflammatory response.
 ETIOLOGY

Streptococcus pneumoniae is most common

TYPICAL ATYPICAL
• S. pneumoniae • M.pneumoniae
• H. influenzae • C. pneumoniae
• S.aureus • Legionella sp.
• K.pneumoniae • Influenza virus
• P. aeruginosa • Adenoviruses
• Metapneumovirus
• Respiratory syncitial virus

Anaerobes – significant role only when an episode of

aspiration has occurred days to weeks before
presentation of pneumonia
 Atypical

Cannot be cultured on standard media or seen on

Gram’s stain
Intrinsically resistant to all beta-lactam agents
Treated with :
 macrolide
 Fluoroquinolone
 tetracycline
 INCUBATION PERIOD

FREQUENT ORGANISMS that WARRANT

HOSPITALIZATION:
1. Streptococcus pneumoniae = 1-3 days
2. Mycoplasma pneumoniae = 1-4 weeks
3. Haemophilus influenzae = 2-4 days
4. Enteric gram-negative bacilli = 1-4 days
5. Legionella species = 2-10 days (up to 16 days)
6. Staphylococcus aureus = 4-10 days (variable)
 CLINICAL MANIFESTATIONS

HISTORY
 Febrile
 Tachycardia
 History of chills and/or sweats
 Productive / Nonproductive cough
 Gross hemoptysis – suggestive of CA MRSA pneumonia
 Pleuritic chest pain
 20% GI symptoms: nausea, vomiting, diarrhea
 Fatigue, headache, myalgias, arthralgias
 CLINICAL MANIFESTATIONS

PHYSICAL EXAM
 Increased respiratory rate
 Use of accessory muscles of respiration
 Increased tactile fremitus
 Dullness on percussion
 (+) crackles , bronchial breath sounds
DIFFERENTIALS: DECREASED
DIFFERENTIALS: DULLNESS ON
VOCAL FREMITUS
PERCUSSION
1. Bronchial asthma
1. Pleural effusion
2. Pleural effusion
2. Atelectasis
3. Atelectasis
Pneumonia (consolidation) –
Pneumonia (consolidation) –
dullness
increased fremitus on affected side
 CLINICAL DIAGNOSIS

1. Infectious
2. Noninfectious: acute bronchitis, acute exacerbations
of chronic bronchitis, heart failure, pulmonary
embolism, hypersensitivity pneumonitis, radiation
pneumonitis
 Pneumatocele

Upper lobe Cavity

 ETIOLOGIC DIAGNOSIS
The etiology of pneumonia usually cannot be
determined solely on the basis of clinical
presentation. Except for CAP patients admitted
to the ICU
No data exist to show that treatment directed at a
specific pathogen is statistically superior to
empirical therapy.
 DIAGNOSTICS
Chest Radiography
 DIAGNOSTICS
Chest Radiography
 DIAGNOSTICS

Gram stain and culture of sputum

Blood cultures
Urinary agents
PCR
Serology – Specific IgM titers
Biomarkers
 Gram stain and culture of sputum

Gram’s stain is to ensure that a sample is suitable for

culture.
 >25 neutrophils and <10 squamous epithelial cells per low-
power field.
Yield of positive cultures: < 50%
Deep-suction aspirate/BAL sample: high yield on
culture when sent to lab ASAP
“Identification of an unexpected pathogen – allows
narrowing of initial empirical regimen”
 Blood cultures

Yield: LOW! (5-14%) – even when collected before

antibiotics given
Strep pneumoniae – most frequently isolated pathogen
No longer considered de rigueuer for all hospitalized CAP
patients – due to low yield and lack of significant impact on
outcome
Except for HIGH RISK patients:
 Neutropenia sec to pneumonia
 Asplenia
 Complement deficiencies
 Chronic liver dse
 Severe CAP
 Urinary agents

1. Legionella antigen in urine – detects only Legionella

pneumophila serogroup 1 (accounts for most
community-acquired cases of Legionnaire’s disease
in the US)
2. Pneumococcal urine antigen test – detects
pneumococcal antigen in urine

Test Sensitivity Specificity

Legionella 90% 99%

Pneumococcal 80% >90%

 PCR

Amplifies microorganism’s DNA or RNA

1. PCR of nasopharyngeal swabs – standard
test for diagnosis of respiratory viral
infection
2. Nucleic acid of Legionella species, M.
pneumoniae, C. pneumoniae,
mycobacteria
 Serology

Fourfold rise in specific IgM antibody titer between

acute and convalescent phase serum samples –
diagnostic of infection with the pathogen in question
 Biomarkers

1. CRP – identification of worsening dse or tx failure

2. Procalcitonin – determining the need for
antibacterial tx
 SITE OF CARE

There are currently two sets of criteria:

1. Pneumonia Severity Index (PSI) - a
prognostic model used to identify patients at low
risk of dying
2. CURB-65 criteria - a severity-of-illness score.
Neither PSI nor CURB-65 is accurate in determining
the need for ICU admission.
Septic shock or respiratory failure in the emergency
department is an obvious indication for ICU care.
Pneumonia Severity Index (PSI)
CURB-65 criteria
 TREATMENT

1. LOW RISK CAP

2. M O D E R A T E R I S K C A P
3. H I G H R I S K C A P
LOW RISK CAP
MODERATE RISK CAP
MODERATE RISK CAP
HIGH RISK CAP
HIGH RISK CAP
RESPONSE TO TREATMENT
FAILURE TO IMPROVE
DE-ESCALATION OF EMPIRIC ANTIBIOTIC

In general, when
switching to oral
antibiotics, either the
same agent as the
paranteral antibiotic or
an antibiotic from the
same drug class should
be used.
 WHEN TO
DISCHARGE
THE
PATIENT
PATIENT EDUCATION
 REFERENCES

Harrisons 19th edition, chapter 151, p.803-813,

PCCP CAP Guidelines 2016