CASE DISCUSSION

CC ERIKA JOHANNA
TAADA

FINAL DIAGNOSIS
COMMUNITY
ACQUIRED
PNEUMONIA PTB
5

WHY
COMMUNIT
Y ACQUIRED
PNEUMONIA
-MR?

1. INFECTION OF THE LUNG

A. aspiration from the oropharynx most
common
B. inhalation as contaminant droplets
C. Hematogenous spread or contiguous
extension
D. Mechanical Factors:
Hairs and turbinates of the nares
Branching architecture of the tracheobronchial tree
Gag reflex and cough mechanisms
Alveolar macrophage

INFLAMMATORY RESPONSE INITIATED

bacteria enter the lower
respiratory tract
adhere to the walls of
bronchi and bronchioles
multiply extracellularly

trigger inflammation

alveolar air spaces fill with an

exudative fluid (i.e., rich in
protein)
Inflammatory cells
(neutrophils during the acute
phase, later macrophages and
lymphocytes during the
chronic phase)
subsequently invade the walls
of the alveoli

infect type II alveolar cells and adhere to alveolar

walls
outpouring of fluid, red and white blood cells, and
fibrin from the circulation
consolidation of the lung
Fluid in the lower airways creates a medium
multiplication of bacteria and spread of infection
through pores of Kohn into adjacent regions of the
lung.

SIGNS AND SYMPTOM PRESENTED BY V.M

productive cough with yelowish expectorant

Difficulty of breathing
Crackles on both lower lung fields
hemoptysis

1. PRODUCTIVE COUGH WITH YELOWISH EXPECTORANT

Cough, particularly cough

with productive of
sputum, is the most
consistent presenting
symptom of pneumonia
as presented by our
patient.

DIFFICULTY OF BREATHING

significant hypoxemia and hypercapnia thick, inflammatory exudate (or pus) collects
in the alveolar spaces and interferes with the
diffusion of oxygen and carbon dioxide

CRACKLES ON BOTH LOWER LUNG FIELDS

are discontinuous, explosive, "popping" sounds
heard when an obstructed airway suddenly opens
and the pressures on either side of the obstruction
suddenly equilibrates resulting in transient, distinct
vibrations in the airway wall.
The dynamic airway obstruction can be caused by
either accumulation of secretions within the airway
lumen or by airway collapse caused by pressure
from inflammation or edema in surrounding
pulmonary tissue

HEMOPTYSIS
Vascular congestion is followed by red hepatization of
the lung where alveoli are filled with blood-tinged
fluid and bacteria to which neutrophils and fibrin are
added. This results in the production of the rustcolored, purulent sputum

PATHOLOGY
series of pathologic changes:
Edema phase proteinaceous exudates and often bacteria in the
alveoli
Red hepatization phase presence of erythrocytes in the cellular
intraalveolar exudates
Gray hepatization no new erythrocytes are extravasating and
those present had been lysed and degraded
Neutrophil is predominant, fibrin deposition is abundant,
bacteria disappeared
Successful containment of infection and improvement of gas
exchange

Resolution the macrophage is the dominant cell type in

the alveolar space

COMMUNITY-ACQUIRED PNEUMONIA
Is the 3rd leading cause of morbidity
( 2001) and
mortality ( 1998 ) in filipinos based from the
Philippine Health Statistics of the DOH.
Differential diagnosis
Infectious:
non infectious: acute bronchitis, acute
exacerbation of chronic bronchitis, heart failure,
pulmonary embolism and radiation pneumonitis

CLINICAL MANIFESTATIONS
Indolent to fulminant
Mild to fatal in severity
Fever, tachycardia, chills and sweats,
cough , dyspnea, pleuritic chest pain,
nausea, vomiting, diarrhea, fatigue,
headache, myalgias and arthralgias
Pulmonary consolidation, effusion

CLINICAL DIAGNOSIS
1. CHEST XRAY

often necessary to help

differentiate CAP from other
conditions
serve as baseline and may
include risk factors for
increased severity
( cavitation or multilobar
involvement)

2.CT scan
rarely necessary but
maybe of value in a patient
with suspected obstructive
pneumonia cause by a
tumor or foreign body.

3. GRAM STAIN AND CULTURE OF

SPUTUM
ensure that a sample is suitable for
culture
Help to identify certain pathogens
To be adequate for culture, sputum
sample must have > 25% neutrophils
and <10 squamous epithelial cells/lpf
ICU and intubated patient deep suction
aspirate or BAL

OTHERS
BLOOD CULTURES
The yield is disappointingly low
only ~ 5 to 14 % of blood culture from hospitalized
patient with CAP are positive
ANTIGEN TESTS
Legionella urine test
PNEUMOCOCCAL URINE ANTIGEN
RAPID TEST FOR INFLUENZA
DIRECT FLUORESCENT ANTIBODY TEST for influenza
virus

POLYMERASE CHAIN REACTION

available for number of pathogens,
including L. pneumophila and
mycobacteria
SEROLOGY
a fourfold rise in specific IgM antibody
titer between acute and convalescent
phase samples is generally considered
diagnostic of infection with the pathogen
in question.

Why
moderate
RISK?

PULMONARY TUBERCULOSIS

 This was considered because of

1. more than 2 week duration of cough
2. hemoptysis
3. chest Xray
4. CT scan

 Tuberculosis is a disease caused by

Mycobacterium tuberculosis
80% is limited to the lungs
Rest is extrapulmonary
Curable
Transmitted through airborne spread of
droplet nuclei produced by patients with
infectious TB

PATHOGENESIS AND IMMUNITY

Droplet nuclei is aerosolized by coughing,
sneezing, speaking (very small particles)
remain suspended in the air reach terminal
air passages when inhaled mycobacteria
adhere to macrophage phogocytosis
surviving mycobacteria laden macrophages
rupture and release bacillary content

Other Factors:
Intimacy and duration of contact
Degree of infectiousness (Cavitary, sputum with 105-7 AFB/ml)
Shared environment

CLINICAL MANIFESTATIONS
Cough ( >2 weeks)
Coughing up blood
Excessive sweating, especially at night
Fatigue
Fever
Unintentional weight loss
Breathing difficulty
Chest pain
Wheezing

TB - DIAGNOSIS

Chest Xray
- typical upper lobe infiltrate
with cavitation in nonimmunocompromised
patients
- atypical findings with
lower zone infiltrates without
cavity formation

 AFB Microscopy

relatively low sensitivity (40-60%),

inexpensive including AFB smear

Mycobacterial Culture

definitive diagnosis

depends on isolation and identification of M. tuberculosis

from the clinical specimen (4-8 weeks)

Nucleic Acid Amplification

rapid diagnosis with

high specificity and sensitivity (several hours) both AFB

positive/negative PTB or ExtraPTB

Drug susceptibility Testing

done

particularly for drug resistant TB

- Isoniazid and Rifampicin

Tuberculin skin testing

screening for

Latent TB
- low sensitivity and specificity
- no value in diagnosis of active TB

WHO TREATMENT GUIDELINE

TB Category

TB Patients

Alternative TB Treatment Regimens

Initial Phase

New smear + PTB,New smear

PTB w/ extensive parenchymal
involvement / New cases of
severe forms of Extra PTB

II

Sputum smear + relapse/

treatment failure/ treatment
after interruption

III

New smear PTB (other than in

Catergory I; New less severe
forms of extra PTB

Continuation Phase

2HRZE
+
Streptomycin

4 HR

2HRZE
+
Streptomycin

5HRE

2HRZ

4 RH