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```CHAPTER 3
PULMONARY MEDICINE
I. Introduction to Pulmonology
II. Approach to Patients with Pulmonary Conditions
1.
2.
Clinical History and Physical Examination
Diagnostic Procedures
III. Common Pulmonary Conditions
1.
2.
3.
4.
5.
6.
7.
8.
Bronchial Asthma
Chronic Obstructive Pulmonary Disease
Community-Acquired Pneumonia
Health Care-Associated Pneumonia
Pulmonary Tuberculosis
Pleural Effusion
Pneumothorax
Superior Vena Cava Syndrome
79
SECTION 1
INTRODUCTION TO PULMONOLOGY
PULMONOLOGY FORMULAS AND REFERENCE VALUES
To compute the A-a gradient appropriate for age:
Normal A – a gradient =
age
4
+ 4
The A-a gradient is the difference between the alveolar oxygen (PAO 2)
and the arterial oxygen (PaO2)1 computed as follows:
A – a gradient = PAO2 – PaO2
PaO2 is derived from patient’s ABG ; while PAO2 is computed as
follows:
PaCO2
PAO2 = FiO2(Patm- PH2O) – 0.8
The normal A – a gradient for a young person
is -5 -10 mmHg (normally increases with age).
Example: A 60 year old patient should have an
(compared to the A-a gradient appropriate for
age) suggests defect in diffusion, V/Q
mismatch or right-to-lung shunting.
PaO2: arterial oxygen partial pressure: obtained
from ABG
PAO2: alveolar oxygen partial pressure
If FiO2 at room air is 21%, Patm at sea level is 760 mmHg and PH2O is 47
mmHg, the formula for A-a gradient can be simplified to:
PaCO2: arterial carbo dioxide pressure: also
obtained from ABG
5
A – a gradient = 150 – 4 (PaCO2) - PaO2
PaO2
PFR = FiO2
PaO2 – FiO2 RATION (PFR)
PaO2: arterial oxygen partial pressure: obtained
from ABG
FiO2: fraction of inspired oxygen
DESIRED PaO2
If age < 60 years old:
Desired PaO2= 104 – (0.43 x age)
*Used for adjust for ventilator FiO2 settings
If age 60 years and above:
Desired PaO2= 80 – (age – 60)
DESIRED FiO2
Current FiO2 x Computed desired PaO2
Desired FiO2
=
Current PaO2
O2 FLOW SYSTEM
Nasal cannula
OXYGEN FLOW RATES
1
2
3
4
5
6
5-6
6-7
7-8
Current PaO2: obtained from ABG
Computed desired PaO2: obtained
previous formula
using
ESTIMATED FiO2 in %
24
28
32
36
40
44
40
50
60
80
SECTION 2
APPROACH TO PATIENTS WITH PULMONARY CONDITIONS
CLINICAL HISTORY AND PHYSICAL EXAMINATION
I. DYSPNEA
A. Pathogenesis of Dyspnea
DESCRIPTION
Chest tightness or constriction
Air hunger, need to breathe, urge to breathe





Cannot get a deep breath, unsatisfying breath


Heavy breathing, rapid breathing, breathing more

Increased work or effort of breathing
B. Variations of Dyspnea
SYMPTOM

Orthopnea
Paroxysmal nocturnal dyspnea
Acute, intermittent episodes of dyspnea


Chronic persistent of dyspnea

Platypnea

PATHOPHYSIOLOGY
Bronchoconstriction
Interstitial edema (asthma, myocardial ischemia)
Airway obstruction (COPD, uncontrolled asthma)
Neuromuscular disease (myopathy, kyphoscoliosis)
Increased drive to breathe (CHF, pulmonary
embolism, moderate-severe airflow obstruction)
Hyperinflation (asthma, COPD)
Restricted tidal volume (pulmonary fibrosis, chest
wall restriction)
Deconditioning
Common indicator of CHF, mechanical impairment
of the diaphragm associated with obesity, or
asthma triggered by esophageal reflux
Highly suggestive of CHF
More likely to reflect episodes of myocardial
ischemia, bronchospasm, or pulmonary embolism
Typical of COPD, interstitial lung disease, and
chronic thromboembolic disease
Left atrial myxoma or hepatopulmonary syndrome
II. COUGH
A. Duration of cough
DURATION
Acute cough
Subacute cough
Chronic cough
<3 weeks
3-8 weeks duration
>8 weeks
COMMON CAUSES
Respiratory tract infection, aspiration
event, inhalation or noxious chemicals
or smoke
Residuum from a tracheobronchitis,
such as in pertussis or “post-viral
tussive syndrome”
Inflammatory, infectious, neoplastic
and cardiovascular etiologies
B. Differential diagnoses for cough with normal chest physical examination and radiography
 Cough-variant asthma
 Gastroesophageal reflux
 Nasopharyngeal drainage
 Medications (angiotensin converting enzyme [ACE] inhibitors)
III. HEMOPTYSIS
 70-90% due to bronchitis, bronchiectasis, necrotizing pneumonia, tuberculosis (owing to high prevalence and its
predilection to cavity formation)
 “BATTLE CAMP”
o Bronchitis, Bronchiectasis
81


o Aspergilloma
o Tumor
o Tuberculosis
o Lung abscess
o Emboli
o Coagulopathy
o Autoimmune disorders, AVM, Alveolar hemorrhage
o Mitral stenosis
o Pneumonia
The origin of blood can be identified by observing its color
o Bright-red, foamy blood: usually from the respiratory tract
o Dark-red, coffee-colored blood: usually from the gastrointestinal tract
Principles of management:
o Maintain airway patency and oxygenation
o Localize the source of bleeding
o Control hemorrhage: may give racemic epinephrine ET flushing (if intubated), concocted as 1 ampule of
epinephrine in 9 mL normal saline solution, as 2 mL flushing q6
IV. CHEST EXAMINATION FINDINGS
CONDITION
PERCUSSION
Normal
FREMITUS
BREATH
SOUNDS
Vesicular
(lung bases)
VOICE
TRANSMISSION
Normal
SOUNDS
Absent
Resonant
Normal
Dull
Increased
Bronchial
Bronchophony,
Egophony
Crackles
Consolidation or
Atelectasis (with
patent airway)
Consolidation or
Atelectasis (with
blocked airway)
Asthma
Emphysema
Dull
Decreased
Decreased
Decreased
Absent
Resonant
Hyperresonant
Normal
Decreased
Vesicular
Decreased
Normal
Decreased
Pneumothorax
Pleural effusion
Hyperresonant
Dull
Decreased
Decreased
Decreased
Decreased
Decreased
Decreased
Pulmonary mass
Dull
(over the mass)
normal
Normal
normal
Wheezing
Absent or
Wheezing
Absent
Absent or Pleural
Friction Rub
Decreased
(over the mass)
82
DIAGNOSTIC PROCEDURES
DIAGNOSTIC


Chest X-Ray (CXR)
Ultrasound (US)






Computed Tomography
(CT)
Ventilation-Perfusion
(VQ) Lung Scanning
Helical CT and
Multidetector CT
CT Pulmonary
Angiography
Magnetic Resonance
Imaging (MRI)
Pulmonary Angiography
Bronchoscopy
Video-Associated
Thoracoscopic Surgery
(VATS)













DESCRIPTION
Routine chest radiography (posterioanterior and lateral views)
Integral part of the diagnostic evaluation involving the parenchyma, pleura, airways
and mediastinum
Lateral decubitus: determine whether pleural abnormalities represent freely flowing
fluid
Apical lordotic views: visualize disease at the lung apices
Produces images using echoes or reflection of the US beam
Can detect and localize pleural abnormalities
Quick and effective way of guiding percutaneous needle biopsy of peripheral lung,
pleural or chest wall lesions
Allows distinction between densities that would be superimpose on plain
Better in characterizing tissue density and providing accurate size assessment of
lesions
Commonly used for evaluation of pulmonary embolism (PE)
PE produces 1 or more regions of VQ mismatch (e.g. regions in which there is a
defect in perfusion that follows the distribution of a vessel & that is not accompanied
by a corresponding defect in ventilation)
Helical CT: faster scans with improved contrast enhancement and thinner
collimation
Multidetector CT: obtains multiple slices in a single rotation that are thinner
Allows simultaneous detection of parenchymal abnormalities
Test of choice for many clinicians in the evaluation of pulmonary embolism
Role is less well defined than that of CT
Poorer spatial resolutions and less detail of the pulmonary parenchyma
Radiopaque contrast medium is injected through a catheter placed in the pulmonary
artery
Direct visualization of the tracheobronchial tree
Performed usually with flexible fiberoptic instruments
Standard technique for diagnosis and management of pleural and parenchyma lung
disease
83
SECTION 3
COMMON PULMONARY CONDITIONS
BRONCHIAL ASTHMA
I. ETIOPATHOGENESIS
 Syndrome characterized by airflow obstruction that varies markedly, both spontaneously and with treatment
 Associated with airway hyperresponsiveness and airflow inflammation
 Symptoms usually demonstrate reversibility and variability
o Reversibility applies to rapid improvements in FEV1 (or PEF)1 measured within minutes after inhalation of
a rapid-acting bronchodilator or more sustained improvement over days or weeks after controller
treatment
o Variability refers to improvement or deterioration in symptoms and lung function occurring over time
 Mast cells, eosinophils, T-lymphocytes, and neutrophils all play a role in the pathogenesis
II. CLINICAL MANIFESTATIONS
History of variable respiratory symptoms AND confirmed variable expiratory airflow limitation
III. History of Variable Respiratory Symptoms
 Typical symptoms include cough, dyspnea, shortness of breath and wheezing
o May be worse at night and in the early morning hours
o Triggered by exercise, laughter, allergens and cold air
o Often appear or worsen with viral infections
 Signs include rhonchi & wheezing throughout the chest but may be normal when asthma is controlled
III. Evidence of Variable Expiratory Airflow Limitation
 At least once during the diagnostic process when FEV1 is low, confirm that FEV1 /FVC is reduced (it is normally
 Document that variation in lung function is greater than in healthy people (examples include the following):
o FEV1 increases by >12% and 200 mL after inhaling a bronchodilator (bronchodilator reversibility)
o Average diurnal PEF variability is >10%
o FEV1 increases by >12% and 200 mL from baseline after 4 weeks of anti-inflammatory treatment
 PEF variability is calculated from twice daily readings (best of 3 each time), averaged over 1-2 weeks:
Day’s highest PEF – Day’s lowest PEF
PEF Variability =
mean of the day’s highest and lowest PEF
III. DIAGNOSIS
A. Classification of Asthma Severity by Level of Control
CONTROLLED
(all of the following)
Daytime Symptoms
None (2x or less/week)
Limitation of Activities
None
Nocturnal Symptoms
None
(Awakening)
Need for Reliever
None (2x or less/week)
Lung Function
Normal
Exacerbation
None
B. Asthma Phenotypes
PHENOTYPE
Allergic Asthma





PARTYLY CONTROLLED
(any measure present)
>2x/week
Any
Any
>2x/week
<80% predicted
1 or more per year
UNCONTROLLED
Three or more symptoms of
partly controlled asthma in
any week
One in any week
DESCRIPTION
Most easily recognizable phenotype
Most often commences in childhood
Associated with a personal or family history of atopy
(eczema, allergic rhinitis, food and drug allergy)
Eosinophilic airway inflammation
Responds well to inhaled corticosteroids (ICS)
84



Non-allergic Asthma
Late-onset Asthma


Asthma with Fixed Airflow Limitation
Neutrophilic or paucigranulocytic airway inflammation
Less responsive to ICS
Common in women, presenting symptoms usually in
Requires higher doses of ICS or are relatively refractory to
ICS
Seen in patients with long-standing asthma who develop
fixed airflow limitation due to airway wall remodeling
IV. MANAGEMENT
 Goals of asthma therapy:
o Minimal (ideally no) chronic symptoms, including nocturnal symptoms
o Minimal (infrequent) exacerbations
o No emergency visits
o Minimal (ideally no) use of as-required B2-agonist
o No limitations on activities, including exercise
o (near) normal PEF
o Minimal (or no) adverse effects from medicine
A. Pharmacologic Therapy for Asthma
DRUG CLASS
EXAMPLES
MECHANISM OF ACTION
EFFECTS
RELIEVERS

Short Acting B2
Agonists
(SABA)
Salbutamol
Procaterol
Terbutaline
Albuterol




Short
Acting
Anticholinergics
Ipratropium
Methylxanthines
Theophylline
Aminophylline


increasing cAMP, causing
bronchodilation
Rapid onset of
bronchodilation
Best used to relief of
symptoms
No effect on chronic
inflammation
Muscarinic receptor
antagonists
Inhibit only the cholinergic
reflex components and
thereby less effective than
B2-agonists
Inhibit phosphodiesterase
activity causing increase in
cAMP levels and
bronchodilation


Tremors and palpitations
(usually in the elderly)
Minimal decrease in serum
K+


Dry mouth (most common)
Urinary retention and
glaucoma may be
observed in the elderly

Nausea, vomiting and
Arrhythmia, seizures and
death at high concentration

CONTROLLERS

Inhaled
Corticosteroids
(ICS)
Beclomethasone
Budesonide
Fluticasone
Systemic
Steroids
Prednisone
Methylprednisolone
Hydrocortisone
Long Acting B2
Agonists
Formoterol
Salmeterol

Most effective antiinflammatory agents for
asthma control
Reduce inflammatory cell
numbers and eosinophils in
airway mucosa

Useful for treatment of acute
exacerbations

Improve asthma control and
reduce inflammation when

Hoarseness / dysphonia
and oral candidiasis

Truncal obesity, easy
bruisability, osteoporosis,
DM, HPN, gastric
ulceration, proximal
myopathy, depression,
cataracts
Should not be given in the
absence of ICS

85
(LABA)
Bambuterol
allowing lower doses of ICS
to be given

Leukotriene
Modifying
Drugs
Montelukast
Zafirlukast
Zileuton

Cromones
Cromolyn sodium
Nedocromil sodium

Inhibit mast cell and sensory
nerve activation
Anti-IgE
Omalizumab

Inhibits IgE-mediated
Block leukotriene receptors
(montelukast, zafirlukast) or
inhibit lipoxygenase
(zileuton)




Less effective than ICS in
controlling asthma and
have less effect on airway
inflammation
therapy in some patients
not controlled with low
doses of ICS
Very short duration of
action needing frequent
dosing
Favorable safety profile
Very expensive
B. Initial Controlled Treatment
 Asthma treatment is a continuous cycle: assess, adjust treatment and review response
 For the best outcomes, regular controller treatment should be initiated as soon as possible after the diagnosis of
 After starting initial controller treatment, review response after 2-3 months, or according to urgency
o Consider stepping up if: uncontrolled symptoms, exacerbations or risks
o Consider stepping down if: symptoms controlled for 3 months, low risk for exacerbations
Indicated only if:
Symptoms are rare
Step 1
As-needed SABA with no controller
No night-walking due to asthma
No exacerbations in the last year
Normal FEV1
Step 2
Low-dose ICS + as-needed SABA
Step 3
Low-dose ICS/LABA + as-needed SABA or
ICS/Formoterol maintenance + reliever therapy
Step 4
Low-dose ICS/Formoterol maintenance + reliever therapy, or
Medium dose ICS/LABA + as-needed SABA
Step 5
Refer for expert investigation
Add-on treatments: anti-IgE (Omalizumab), low dose oral steroids
C. Non-Pharmacologic Therapy of Asthma
 Smoking cessation
 Regular physical activity
 Occupational aspects
 Breathing techniques
V. CLASSIFICATION AND MANAGEMENT OF EXACERBATIONS
MILD OR MODERATE
SEVERE
LIFE THREATENING
Clinical
Talks in phrases
Talks in words
manifestations
Prefers sitting to lying
Sits hunched forward
Not agitated
Agitated
Drowsy,
Respiratory rate
Increased
>30/min
Confused,
Accessory
Not used
Used
Silent chest
muscles
Pulse rate
100-120 bpm
>120 bpm
O2 saturations
90-95%
<90%
Peak Expiratory
>50% predicted or best
< 50% predicted or best
Flow (PEF)
SABA
Transfer to acute care facility
Treatment
Ipratropium bromide
SABA
Prednisolone 1mg/kg PO
Ipratropium bromide
86
Controlled oxygen
Controlled oxygen
Oral or IV corticosteroids
Consider IV magnesium
Consider high dose ICS
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)
I. ETIOPATHOGENESIS
 Characterized by expiratory airflow limitation that is not fully reversible (hallmark: airflow obstruction)
 Unusual in the absence of smoking or prior history of smoking, except for patients with A1-antitrypsin deficiency
 Elastase-Antielastase Hypothesis: remains a prevailing mechanism for its pathophysiology
A. The Pathological Changes include:
 Chronic inflammation
 Increased numbers of specific inflammatory cell types in different parts of the lung
 Structural changes resulting from repeated injury and repair
B. Encompasses the Following Conditions:
 Emphysema: anatomically-defined condition characterized by enlargement and destruction of alveoli “pink
puffers”)
 Chronic bronchitis: clinical condition characterized by chronic cough and phlegm (“blue bloaters”)
 Small airways disease: condition where bronchioles are narrowed
II. CLINICAL MANIFESTATIONS
CARDINAL SYMPTOMS


Most common symptoms:
Cough, sputum production, exertional
dyspnea






SIGNS
May be normal in early stages
Pink puffers (predominantly emphysema): thin, non-cyanotic,
prominent use of accessory muscles
Blue bloaters (predominantly chronic bronchitis): heavy and cyanotic
“Tripod position”: to facilitate use of accessory muscles
Signs of hyperinflation: barrel chest, enlarged lung volumes on
percussion (hyperresonance)
Others: pursed-lip breathing, expiratory wheezing, systemic wasting,
weight loss
Signs of cor pulmonale (bipedal edema, ascites) in severe cases
Clubbing is not a sign of COPD and should alert the clinician to other
causes of clubbing
III. DIAGNOSIS
 A clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum
production, and a history of exposure to risk factors for the disease
 Risk factors: tobacco smoke (including popular local preparations), smoke from home cooking and heating
fuels, occupational dusts and chemical
DIAGNOSTIC TEST
 Required to make the diagnosis
 Post-bronchodilator FEV1/FVC <0.70 confirms presence of persistent
airflow limitation
 Degree of reversibility of airflow limitation after bronchodilators /
steroids is no longer recommended (it has never been shown to add
Spirometry
to the diagnosis, differential diagnosis, or to predicting the response
to long-term treatment with bronchodilators or corticosteroids)
 FEV1, FEV1/FVC and all other measures of expiratory airflow are
reduced
 TLC, FRC and RV may be increased indicating air trapping
 DLCO may be reduced
 Useful for excluding other differential diagnoses
87




CT scan


Pulse oximetry

Arterial blood gas (ABG)




IV. CLASSIFICATION OF COPD
PATIENT
CHARACTERISTIC
A
B
C
D
Low risk
Less symptoms
Low risk
More symptoms
High risk
Less symptoms
High risk
More symptoms
Low flattened diaphragms, increase in the volume of retrosternal
airspace (hyperinflation)
Hyperlucent lung zones with possible bullae formation and diminished
vascular markings
Not routinely requested
May be helpful when the diagnosis is in doubt to rule out concomitant
diseases
Useful if surgical procedure such as lung volume reduction is
contemplated
To evaluate a patient’s oxygen saturation and need for supplemental
oxygen therapy
Should be used to assess all stable patients with FEV1<35%
predicted or with clinical signs suggestive of respiratory failure or right
heart failure
If peripheral saturation is <92%, ABGs should be assessed
Resting or exertional hypoxemia
In long-standing disease, may have chronically increased arterial
PaCO2 but metabolic compensation (increased HCO 3) maintains pH
near normal
SPIROMETRIC
CLASSIFICATION
GOLD 1-2
EXACERBATIONS PER
YEAR
<1
mMRC
GOLD 1-2
<1
>2
GOLD 3-4
>2
0-1
GOLD 3-4
>2
>2
0-1
A. Classification based on Severity of Airflow Limitation in COPD using Spirometry (Post-Bronchodilator FEV1)
 Spirometry should be performed after the administration of an adequate dose of a short-acting inhaled
bronchodilator (to minimize variability)
STAGE
CLINICAL FINDINGS
SPIROMETRY FINDINGS
FEV1/FVC
FEV1
 Chronic
cough
and
GOLD 1
FEV1> 80% predicted
sputum production
Mild
 Patient unaware that lung
function is abnormal
 Chronic cough and sputum
production
GOLD 2
FEV1 50 to <80%
 Shortness of breath on
Moderate
predicted
exertion
FEV1 / FVC
 Stage patients typically seek
<0.70
medical attention
 Greater shortness of breath
GOLD 3
FEV130 to <50%
 Reduced exercise capacity
Severe
predicted
 Fatigue
 Repeated exacerbations
 Signs
or
symptoms
of
GOLD 4
FEV1<30% predicted
respiratory failure (PaO2< 60
Very Severe
mmHg + PaCO2>50 mmHg)
 Cor pulmonale
88
B. Classification Based on Exacerbation
 Exacerbation of COPD: defined as an acute event characterized by worsening of the patient’s
respiratory symptoms that is beyond normal day-to-day variations and leads to a change in medication
 Best predictor of having frequent exacerbations (2 or more per year) is a history of previously treated
events
C. Modified Medical Research Council (mMMRC) Questionnaire for Assessing the Severity of Breathlessness
mMMRC
DESCRIPTION
0
I only get breathless with strenuous exercise
1
I get short of breath when hurrying of the level or walking up a slight hill
2
I walk slower than people of the same age on the level because of breathlessness, or I
stop for breath when walking on my own pace on the level
3
I stop for breath after walking 100 meters or after a few minutes on the level
4
I am too breathless or I am breathless when I’m dressing or undressing
V. OVERVIEW OF MANAGEMENT
A. Only Three Interventions have been demonstrated to influence the natural history of COPD
 Biggest impact in the natural history of COPD
 Nicotine replacement therapy (gum, inhaler, nasal spray, transdermal
Smoking Cessation
patch) reliably increases long term smoking abstinence rates
 Brief (3-minute) period of counseling to urge a smoker to quit results in
smoking cessation rates of 5-10%
 Only pharmacologic therapy demonstrated to unequivocally decrease
Oxygen Therapy
mortality rates in COPD
 For chronically hypoxemic patients
 >15 hours / day (long term oxygen therapy)
Lung Volume Reduction Surgery
 Segmentectomy or lobectomy of focal emphysematous areas of the
lung
B. Pharmacologic Therapy for Stable COPD
 None of the existing medications for COPD have been shown to modify the long-term decline in lung function
 Bronchodilator medications are central to the symptomatic management of COPD (principal bronchodilator
treatment includes B2-agonists, anticholinergics and methylxanthines)
MEDICATIONS
 Alters airway smooth muscle tone improving
emptying of the lungs
 Sinus tachycardia
 Effects usually wear off within 4-6 hours (short
acting) and >12 hours (long acting)
 Arrhythmias
Beta2 – Agonists
 Regular treatment with LABA is more effective
 Tremors
and convenient than treatment with SABA
 Hypokalemia
 Appears to provide subjective benefit in acute
episodes but is not necessarily helpful in stable
disease
 Blocks acetylcholine’s effect on muscarinic
receptors
 Dryness of the mouth
 Example:
ipratropium,
oxitropium,
and
Anticholinergics
tiotropium bromide
 Bitter metallic taste
 Bronchodilating effects of short-acting inhaled
 Arrhythmias
anticholinergics lasts longer than that of shortacting B2-agonists
 Tachycardia
 Acts as nonselective phosphodiesterase
 Arrhythmias
Methylxanthines
inhibitor
 Seizures
 Examples: theophylline, doxofylline
 Insomnia
Inhaled
 Addition of ICS to bronchodilator treatment
 Hoarseness
corticosteroids
appropriate for:
 Oral candidiasis
89
o

Symptomatic patients with FEV1<50%
predicted (Stages III and IV)
o Repeated exacerbations
Chronic treatment with systemic glucocorticoids
should be avoided
VI. MANAGEMENT OF STABLE COPD
A. Pharmacologic Management of COPD
PATIENT
RECOMMENDED FIRST
GROUP
CHOICE
A
B
ALTERNATIVE CHOICE
SAMA pm
or
SABA pm
LAMA
or
LABA
or
SABA and SAMA
LAMA
or
LABA
LAMA and LABA
C
ICS + LABA
or
LAMA
D
ICS + LABA
and/or
LAMA
LAMA and LABA
or
LAMA and PDE-4 inhibitor
or
LABA and PDE-4 inhibitor
ICS + LABA and LAMA
or
ICS + LABA and PDE-4 inhibitor
or
LAMA and LABA
or
LAMA and PDE-4 inhibitor
OTHER POSSIBLE
TREATMENT
Theophylline
SABA and/or SAMA
Theophylline
SABA and/or SAMA
Theophylline
Carbocisteine
SABA and/or SAMA
theophylline
SAMA: Short acting muscarinic antagonist (e.g., Ipratropium)
SABA: Short acting beta agonist (e.g. Salbutamol)
LAMA: Long acting muscarinic agonist (e.g., Tiotropium)
LABA: Long acting beta agonist (e.g., Salmeterol)
ICS: Inhaled corticosteroid (e.g. Budesonide)
PDE-4 inhibitor (e.g., Roflumilast)
B. Non-Pharmacologic Management of COPD
PATIENT GROUP
ESSENTIAL
RECOMMENDED
A
Smoking cessation
Physical activity
B-D
Smoking cessation
Pulmonary rehabilitation
Physical activity
DEPENDING ON LOCAL
GUIDELINE
Flu vaccination
Pneumococcal vaccination
Flu vaccination
Pneumococcal vaccination
VII. MANAGEMENT OF ACUTE EXACERBATIONS
 Exacerbation: event in the natural course of the disease characterized by a change in patient’s baseline
dyspnea, cough, and/or sputum that is beyond normal day-to-day variations, is acute in onset, and may warrant a
change in regular medication in patients with underlying COPD
 Change in mental status is the most important sign of a severe exacerbation in patients with very severe COPD
A. Management of Severe but Not Life-Threatening Exacerbations of COPD at the ER
 Assess severity of symptoms, blood gases, and CXR
 Administer controlled oxygen therapy and repeat ABG after 30-60 minutes
 Increase doses and/or frequency of bronchodilator use
 Add oral or IV glucocorticoids
 Consider antibiotics (oral or occasionally IV) when there are signs of bacterial infection
 Consider non-invasive mechanical ventilation
90
B. Therapy for Acute Exacerbation
MANAGEMENT
Bronchodilators
 Inhaled B-agonists often with addition of anticholinergic agent
 Frequency depends on severity of exacerbation
 Bacteria frequently implicated in exacerbations: Streptococcus pneumoniae,
Antibiotics
Haemophilius influenza, Moraxella catarrhalis
 Most clinicians treat patients with moderate or severe exacerbations with
antibiotics, even in the absence of data implicating a specific pathogen
 Reduces hospital stay, hastens recovery and reduces chances of subsequent
Glucocorticoids
exacerbations / relapses
 Prednisone 40 mg/day or its equivalent for 5 days
 Most common acute complication for steroids: hyperglycemia
Oxygen
 Maintain O2 saturation > 90%
 Administration of oxygen does not reduce minute ventilation
C. Indications for Ventilator Support
NON-INVASIVE VENTILATION
Selection Criteria
 Moderate to severe dyspnea with use of
motion
 Moderate to severe acidosis (pH <7.35) and/or
hypercapnia (PaCO2>45mmHg)
 RR >25/min
Exclusion Criteria (any may be present)
 Respiratory arrest
 Cardiovascular instability
 Change in mental status; uncooperative patient
 High aspiration risk
 Viscous or copious secretions
 Recent facial or gastroesophageal surgery
 Craniofacial trauma
 Fixed nasopharyngeal abnormalities
 Burns
 Extreme obesity
INVASIVE MECHANICAL VENTILATION
Indications
 Unable to tolerate NIV or NIV failure
 Severe dyspnea with use of accessory muscles
 RR >35/min
 Life-threatening hypoxemia
 Severe acidosis (pH <7.25) and/or hypercapnia
(PaCO2>60 mmHg)
 Respiratory arrest
 Somnolence, impaired mental status
 Cardiovascular complications
 Other complications (e.g., metabolic abnormalities,
sepsis,
pneumonia,
pulmonary
embolism,
barotrauma, massive pleural effusion)
D. Discharge Criteria
 Inhaled beta-agonist use no more frequent than q4h
 Patient is able to walk across room
 Patient able to eat and sleep without frequent awakening by dyspnea
 Patient has been clinically stable for 12-24 hours
 ABG have been stable for 12-24 hours
 Patient (or home caregiver) fully understands the use of meds
 Follow-up plans have been finalized and home care arrangements have been completed
COMMUNITY-ACQUIRED PNEUMONIA (CAP)
I. ETIOPATHOGENESIS
 Lower respiratory tract infection (pulmonary parenchyma) acquired in the community within 24 hours to less than
2 weeks
 Results from the proliferation of microbial pathogens at the alveolar level and the host’s response to those
pathogens
 Most common access of microorganisms to the lower respiratory tract is through aspiration from the oropharynx
 Classic pneumonia (lobar pneumococcal) evolves through a series of changes
91
PHASE

Edema




Red Hepatization

Gray Hepatization


Resolution (Final
Phase)
DESCRIPTION
Initial phase with the presence of a proteinaceous exudate and often of bacteria
in the alveoli
Erythrocytes in the cellular intraalveolar exudate
Neutrophil influx is more important from the standpoint of host defense
Bacteria are occasionally seen in pathologic specimens
No new erythrocytes are extravasating and those already present have been
The neutrophilis the predominant cell, fibrin deposition is abundant and bacteria
have disappeared
This phase corresponds with successful containment of the infection and
improvement in gas exchange
Macrophage reappears as the dominant cell type in the alveolar space and the
debris of neutrophils, bacteria and fibrin has been cleared, as has the
inflammatory response
II. CLINICAL MANIFESTATIONS
 Commonly presents with acute cough, abnormal vital signs of tachypnea, tachycardia, and fever with at least one
abnormal chest finding of diminished breath sounds, rhonchi, crackles or wheezes
III. DIAGNOSIS
A. Classification and Disposition
LOW-RISK CAP
Stable
 RR <30/min
Vital Signs
 PR <125bpm
 Temp 36-40oC
 BP > 90/60mmHg

Features


Chest X-Ray
Disposition




No altered mental
state of acute onset
No suspected
aspiration
No or stable
comorbids
Localized infiltrates
No pleural effusion
No abscess
outpatient
MODERATE-RISK CAP
Unstable
 RR > 30/min
 PR >12bpm
 Temp > 40oC or
<36oC
 BP < 90/60 mm/Hg
 Altered mental state
of acute onset
 Suspected
aspiration
 Decompensated comorbidities
 Multilobar infiltrates
 Pleural effusion
 Abscess
B. Diagnostics for CAP
DIAGNOSTICS


Microbiologic Studies
(sputum and blood cultures)
Invasive Procedures
(e.g.,
transtracheal,
transthoracic,
biopsy,
bronchoalveolar lavage, protected brush specimen)




HIGH-RISK CAP
Any of the criteria under
Moderate Risk CAP, plus:
 Severe sepsis and
septic shock
 Need for
mechanical
ventilation

Essential in the diagnosis of CAP, assessing
severity, differentiating pneumonia from other
conditions and in prognostication
Best radiologic evaluation consists of standing
posterioanterior and lateral views of the chest
Does not predict the likely etiologic agent
Optional in low-risk CAP
Necessary in moderate- and high-risk CAP
Options
for
non-resolving
pneumonia,
immunocompromised patients and in whom no
adequate respiratory specimens can be sent
despite sputum induction and routine diagnostic
testing
92
IV. MANAGEMENT
 For patients requiring hospitalization, empiric therapy should be initiated as soon as possible after a diagnosis
 Empiric microbial therapy for CAP:
RISK STRATIFICATION
POTENTIAL PATHOGENS
EMPIRIC THERAPY
Previously healthy:
Amoxicillin or extended macrolides
(suspected atypical pathogen)
Streptococcus pneumoniae
Haemophilus influenza
With stable comorbid illness:
Chlamydphila pneumoniae
β-lactam / β-lactamase inhibitor
Low-Risk CAP
Mycoplasma pneumoniae
combination (BLIC) or secondMoraxella catarrhalis
generation oral cephalosporin +
Enteric Gram-negative bacilli
extended macrolides
(among those with co-morbids)
Alternative:
Third-generation oral cephalosporin
+ extended macrolide
Streptococcus pneumoniae
Haemophilus influenza
IV non-antipseudomonal β-lactam
Chlamydphila pneumoniae
(BLIC, cephalosporin or carbapenem)
Mycoplasma pneumoniae
+ extended macrolide
Moderate-Risk
Moraxella catarrhalis
or
CAP
Enteric Gram-negative bacilli
IV non-antipseudomonal β-lactam +IV
Legionella pneumophila
extended macrolide or IV respiratory
Anaerobes (risk of aspiration)
FQ
No risk for P. aeruginosa:
High-Risk CAP
Streptococcus pneumoniae
Haemophilus influenza
Chlamydphila pneumoniae
Mycoplasma pneumoniae
Moraxella catarrhalis
Enteric Gram-negative bacilli
Legionella pneumophila
Anaerobes (risk of aspiration)
Staphylococcus aureus
Pseudomonas aeruginosa
IV non-antipseudomonal β-lactam +IV
extended macrolide or IV respiratory
FQ
With risk for P. aeruginosa:
IV antipneumococcal antipseudomonal
β-lactam + IV extended macrolide +
aminoglycoside
or
IV antipneumococal antipseudomonal
β-lactam + IV ciprofloxacin/levofloxacin
(high-dose)
1. Extended macrolides: azithromycin dehydrate, clarithromycin
2. Oral β-lactam/β-lactamase inhibitor (BLIC): amoxicillin-clavulanic acid, amoxicillin-sulbactam, sultamicillin
3. Oral second-generation cephalosporin: cefaclor, cefuroxime axetil
4. Oral third-generation cephalosporin: cefdinir, cefixime, cefpodoxime proxetil
5. IV non-antipseudomonal β-lactam (BLIC, cephalosporin or carbapenem): amoxicillin-clavulanic acid, ampicillin-sulbactam, cefotiam,
cefoxitin, cefuroxime Na, cefotaxime, ceftizoxime, ceftriaxone, ertapenem
6. Respiratory fluoroquinolones: levofloxacin, moxifloxacin
7. IV antipneumococal, antipseudomonal β-lactam (BLIC, cephalosporin or carbapenem): cefoperazone-sulbactam, piperacillin-tazobactam,
ticarcillin-clavulanic acid, cefipime, cefpirome, imipenem-cilastatin, meropenem
8. Aminoglycosides: gentamicin, tobramycin, netilmicin, amikacin
V. PNEUMONIA RISK SCORE (CURB-65) PREDICTS MORTALITY IN CAP
C
Confusion of new onset
U
Urea (BUN) > 7 mmol/L (19 mg/dL)
R
Respiratory rate > 30 bpm
B
Blood pressure <90/60 mmHg
65
Age >65 years old
Interpretation:
 0-1: treat as outpatient
93
VI. ASSESSING RESPONSE TO THERAPY
A. Response to therapy is expected within 24-72 hours of initiating treatment:
 Temperature, RR, HR, BP, sensorium, O2 saturation, and inspired oxygen concentration should be monitored
to assess response to therapy
 A patient is considered to have responded to treatment if:
o Fever decreases within 72 hours;
o Temperature normalizes within 5 days; and,
 Follow-up cultures of blood and sputum are not indicated for patients who are responding to treatment
B. De-escalation of antibiotic therapy once the patient is improving, stable and has a functioning GI tract:
 Resolution of fever more than 24 hours
 Less cough and resolution of respiratory distress (normalization of RR)
 Improving WBC count, no bacteremia
 Etiologic agent is not a high-risk (virulent/resistant) pathogen (e.g. Legionella, S. aureus, or gram-negative
enteric bacilli)
 No unstable comorbid condition or life-threatening complications such as MI, CHF, complete heart block, new
atrial fibrillation, supraventricular tachycardia, etc.
 No sign of organ dysfunction such as hypotension, acute mental changes, BUN to creatinine ratio of >10:1,
hypoxemia, and metabolic acidosis
 Patient is clinically hydrated, taking oral fluids and is able to take oral medications
C. Duration of Treatment
ETIOLOGIC ORGANISMS
Most bacterial pneumonias
Enteric Gram-negative pathogens, S. aureus, and P.
aeruginosa
Mycoplasma and Chlamydophila
Legionella
DURATION OF TREATMENT (days)
5-7
14
10-14
14-21
D. Failure to improve after 72 hours of treatment is an indication of reassessment
 Incorrect diagnosis or presence of complicating noninfectious condition (e.g., pulmonary embolism, CHF,
vasculitis, MI)
 A resistant microorganism or an unexpected pathogen that is not covered by the antibiotic of choice
 Antibiotic is ineffective or causing an allergic reaction
 Impaired local or systemic host defenses (e.g., aspiration, endobronchial obstruction, bronchiectasis)
 Local or distant complications of pneumonia (e.g., parapneumonic effusion, empyema, lung absecess, ARDS,
metastatic infection, endocarditis)
 Overwhelming infection
 Slow response in the elderly patient (S. pneumoniae and L. pneumophila)
 Exacerbation of co-morbid illness
 Nosocomial superinfection
E. Hospital Discharge
 In the absence of any unstable coexisting illness or other life-threatening complication, the patient may be
discharged once clinical stability occurs and oral therapy is initiated
1. During the 24 hours before discharge, the patient should have the following characteristics:
 Temperature of 36-37.5oC
 Pulse <100/min
 RR between 16-14/min
 SBP >90 mmHg
 Blood O2 saturation >90%
 Functioning GI tract
 Not needed in patients who are clinically improving
 Recommended during a follow-up visit, approximately 4 to 6 weeks after hospital discharge
94
HEALTH CARE-ACQUIRED PNEUMONIA (HCAP)
I. ETIOPATHOGENESIS
 Transition between classic CAP and typical HAP
A. Ventilator-Associated Pneumonia (VAP)
 The greatest difference between VAP and HCAP/HAP is the return to dependence on expectorated sputum for a
microbiologic diagnosis of VAP, which is further complicated by frequent colonization by pathogens in patients
with HAP or HCAP
 Common pathogenic mechanisms include oropharyngeal colonization with pathogenic bacteria, cross-infection
from other colonized patients, large volume aspiration, microaspiration around ET tub and altered lower
respiratory host defenses
 Clinical manifestations: same in VAP as with any other forms of pneumonia: fever, leukocytosis, increase in
secretions, and pulmonary consolidation on PE, along with a new or changing radiographic infiltrate
NON-MDR PATHOGENS
MDR PATHOGENS
Streptococcus pneumoniae
Pseudomonas aeruginosa
Other Streptococcus spp.
MRSA
Haemophilius 95nfluenza
Acinetobacter spp.
Antibiotic-resistant Enterobacteraceae
MSSA
Antibiotic-sensitive Enterobacteriaceae
Enterobacter spp.
Escherichia coli
ESBL-positive strains
Klebsiella pneumoniae
Klebsiella spp.
Proteus spp.
Legionella pneumophila
Enterobacter spp.
Burkholderia cepacia
Serratia marcescens
Aspergillus spp.
B. Hospital-Acquired Pneumonia (HAP)
 HAP in non-intubated patients, both inside and outside the ICU, is similar to VAP save for the higher frequency of
non-MDR pathogens and better underlying host immunity in non-intubated patients  the lower frequency of
MDR pathogens allows monotherapy in a majority of HAP cases
 The only pathogens that may be more common in the non-VAP population are the anaerobes (due to a higher risk
of macroaspiration)
 More difficult to obtain lower respiratory samples appropriate for culture in non-intubated patients
II. CLINICAL CONDITIONS ASSOCIATED WITH MDR PATHOGENS IN HCAP
 Hospitalization for > 48 hours
 Hospitalization for > 2 days in prior 3 months
 Nursing home or extended-care-facility residence
 Antibiotic therapy in preceding 3 months
 Chronic dialysis
 Home infusion therapy
 Home wound care
 Family member with MDR infection
III. MANAGEMENT
 Once an etiologic diagnosis is made, broad-spectrum empirical therapy can be modified to address the known
pathogen specifically
 Empirical antibiotic treatment of HCAP
WITHOUT RISK FACTORS FOR MDR PATHOGENS
WITH RISK FACTIRS FOR MDR PATHOGENS
Standard recommendation is treatment with three
antibiotics: two directed at P. aeruginosa and one at
Majority can be treated with a single agent
MRSA
A beta-lactam:
Ceftriaxone 2g IV q24
Moxifloxacin 400 mg IV q24
 Ceftazidime 2g IV q8 or Cefepime 2g IV q8-12
Ciprofloxacin 400 mg IV q8
or
Levofloxacin 750 mg IV q24
 Piperacillin/tazobactam 4.5g IV q6, Imipenem
Ampicillin/sulbactam 3g IV q6
500 mg IV q6 or 1g IV q8, plus
Ertapenem 1g IV q24
95
A second agent against gram-negative bacteria:
 Gentamicin or Tobramycib 7 mg/kg IV q24 or
Amikacin 20 mg/kg IV q24, or
 Ciprofloxacin 400 mg IV q8 or Levofloxacin 750
mg IV q24, plus
An agent against gram-positive bacteria:
 Linezolid 600 mg IV q12, or
 Vancomycin 15mg/kg, up to 1 g IV q12
PULMONARY TUBERCULOSIS (PTB)
I. ETIOPATHOGENESIS
 Caused by Mycobacterium tuberculosis
 Most common site for the development of TB is the lungs (85% of patients)
 Most commonly transmitted from person with infectious PTB to others by droplet nuclei, which are aerosolized by
coughing, sneezing or speaking. Aerosolized droplets are 1-5 µm in diameter. A single cough can generate 3000
infective droplets, with as few as 10 bacilli needed to initiate infection
 Most infectious patients: those with cavitary pulmonary disease and laryngeal TB
 Typical TB lesion: epitheloid granuloma with central caseation necrosis
II. CLINICAL MANIFESTATIONS
 In the Philippines, cough of two weeks or more should lead to high index of suspicion for PTB
 Cough may be accompanied by night sweats, weight loss, unexplained fever and chills, chest pain, fatigue and
body malaise
 Absence of fever does not exclude TB
 Physical findings are of little utility in PTB
A. General Classification of Tuberculosis
CLASSIFICATION


Presumptive TB



DEFINITIONS
Cough of at least 2 weeks in an adult (age > 15 y/o)
A child (< 15 y/o) fitting criteria for TB
Any person who presents with symptoms or signs suggestive of TB
Cough of any duration in a high risk individual or a close contact of an
active TB case
Definite case
 A patient with MTB complex identified from a clinical specimen either by
culture or by a newer method such as molecular line probe assay
New case
 Patient who never had treatment for TB or who has taken anti-TB
medications for < 1 month
Retreatment case (patient previously treated with anti-TB drugs for at least 1 month in the past)
 Patient who was previously treated for TB, and was declared cured for has
Relapse
completed treatment; and is now bacteriologically or clinically diagnosed
TB
 Patient who was previously treated for TB, and treatment failed at the end
of the most recent course:
o Sputum smear or sputum culture positive at 5 months or later
Treatment after failure
during treatment
o Clinically diagnosed in a patient in whom sputum studies cannot
be done, without clinical improvement anytime during the course
of treatment
Treatment after lost to follow A patient who returns to treatment with positive bacteriology (smear or
up (TALF)
culture) or clinically diagnosed, following interruption of treatment for two
months or more
Previous treatment outcome
 A previously treated patient whose outcome was not known or not
unknown (PTOU)
documented
96
B. Classification of Tuberculosis based on Anatomical Site Affected
At least 1 (or 2) sputum
specimen positive for AFB,
abnormalities
Patient with sputum culture,
Culture-positive
abnormalities
Patient with positive sputum
Rapid Diagnostic testfor MTB using a rapid
positive
diagnostic test (e.g. Xpert
MTB/Rif) with or without
Two sputum specimens negative for AFB or MTB; but with
clinical or radiologic evidence consistent with active TB and
there is a decision by a physician to treat as tuberculosis
Smear/culture/rapid diagnostic test from an extrapulmonary site positive for AFB
A patient with histologic and/or clinical or radiologic
evidence consistent with active extra-pulmonary TB and
there is a decision by a physician to treat as tuberculosis
Smear-positive
BacteriologicallyConfirmed
Pulmonary TB
Clinically-Diagnosed
Extra-Pulmonary TB
(EPTB)
BacteriologicallyConfirmed
Clinically-Diagnosed
III. DIAGNOSIS
DIAGNOSTICS


Sputum Microscopy for AFB


Sputum TB Culture

Rapid Diagnostic Test (Xpert
MTB/Rif Assay)


At least two sputum specimens should be sent
Sputum collection:
o Two sputum specimens of good quality shall be collected, either
morning specimens, based on the patient’s preference
o The two specimens should be collected at most within 3 days
Primarily recommended for patients at risk for drug resistance
It is recommended in the following smear positive patients:
o All cases of retreatment
o All cases of treatment failure
o All other cases of smear positive patients suspected to have one
or more multi-drug resistant TB
o All household contacts of patients with MDR-TB
o In patients with HIV
Recommended for patients suspected to have PTB whose sputum
smears are negative
Initiating TB treatment based on chest radiographs alone is discouraged
Gene Xpert testing for the presence of Mycobacterium tuberculosis and
Rifampicin resistance
97
Presumptive TB
Cough of at least 2 years in an adult > 15 years old
CXR suggestive of tuberculosis
Cough of any duration in a high risk individual or close contact of an active TB case
Sputum smear microscopy
Positive*
Negative or not done
If not suggestive of TB  Not TB
If suggestive of TB  proceed to nest step
Bacteriology confirmed TB
MTB (+)
Rif-sensitive
Xpert MTB/Rif**
MTB Negative  Not TB
MTB Positive  Next step
History of previous TB treatment?
No
Bacteriologically
confirmed TB
New Case
Yes
MTB (+)
Rif-Resistant
Bacteriologically
confirmed TB
Retreatment
Refer to PMDT\$
Services for
Evaluation
Clinically
Diagnosed TB
Retreatment
MTB/Rif:
Decision of MD or TBDC+?
Either “Not TB” or “Clinically
Diagnosed TB”
Yes
Category I
Treatment
History of
previous TB
treatment?
Category II Treatment
(for Rif-sensitive)
If clinically
diagnosed
TB
No
Clinically
Diagnosed TB
New Case
*Positive: at least 1 (of 2) specimen for acid fast bacilli
** Xpert MTB/Rif: Rapid diagnostic test for the presence of Mycobacteria tuberculosis and Rifampicin resistance
+ TBDC: Tuberculosis diagnostic committee
\$ PMDT: Programmatic Management of Drug-Resistant Tuberculosis (possible MDR-TB treatment if Rifampicin Resistant TB)
98
IV. MANAGEMENT
A. Treatment Regimen for TB
CATEGORY

I

Ia


II

IIa

Drug
Resistant
TB

TB PATIENTS
ALTERNATIVE TB TREATMENT REGIMEN
Initial Phase
Continuation Phase
New pulmonary TB (bacteriologicallyconfirmed or clinically diagnosed)
New extra-pulmonary TB (bacteriologicallyconfirmed or clinically-diagnosed), except
CNS / bones or joints
New extra-pulmonary TB (CNS / bones or
joints)
Pulmonary or extra-pulmonary, previously
treated drug-susceptible TB (whether
bacteriologically-confirmed or clinicallydiagnosed), except CNS / bones or joints
o Relapse
o Treatment after failure
o Treatment after lost to follow-up
(TALF)
o Previous treatment outcome
unknown (PTOU)
o Other
Extra-pulmonary (CNS / bones or joints),
previously treated, drug susceptible TB
(whether bacteriologically-confirmed or
clinically-diagnosed)
Standard regime drug-resistant (SRDR):
rifampicin resistant TB or multi-drug
resistant TB
XDR TB regimen: extensively drugresistant TB
2 HRZE*
4 HR or 4HRE*
2 HRZE
10 HR
2 HRZES and 1
HRZE
5 HRE
2 HRZES and 1
HRZE
9 HRE
Individualized based on previous treatment
courses and drug sensitivity testing
*if with cavitary disease, give streptomycin IM alternate days (60 days) instead of ethambutol
# based on the WHO guideline, in populations with known or suspected high levels of isoniazid resistance, new TB patients may receive HRE as
therapy in the continuation phase as an acceptable alternative to HR
B. Drugs used for Tuberculosis
DRUG
DOSE
(daily)
Isoniazid
(H/INH)
5 mg/kg,
max 300 mg
MECHANISM OF ACTION




Rifampicin
(R)
10 mg/kg,
max 600 mg




Pyrazinamide
(Z)
25 mg/kg,
max 2 g


Ethambutol
(E)

15 mg/kg
Inhibits fatty acid synthase and mycolic acid synthesis
Excellent bactericidal activity against both intracellular and extracellular
actively dividing MTB
Bacteriostatic against slowly dividing organisms
Binds to and inhibits mycobacterial DNA-dependent RNA polymerase
thereby blocking RNA synthesis
Has both intracellular and extracellular bactericidal activity, both in
dividing and non-dividing MTB
Also has sterilizing activity
Most active antimycobacterial agent available and therefore the
cornerstone of first-line TB treatment
Exact mechanism is unclear (fatty acid synthetase-) may be the primary
target)
More active against slowly replicating organisms than against actively
replicating organisms
Active only in acidic environment (pH<6.0) and are found within
phagocytes or granulomas
Inhibits arabinosyltransferases involved in cell wall synthesis, which
probably inhibits the formation of arabinogalactan and
lipoarabinomannan
99



Streptomycin
(S)
15 mg/kg,
max 1 g

Bacteriostatic antimycobacterial agent which provides synergy with
other drugs
Least potent against MTB
Inhibits protein synthesis by binding at a site in #)S mycobacterial
ribosome
Bactericidal against dividing MTB but has only low-level early
bactericidal activity
C. Managing Side-Effects
SIDE EFFECTS
DRUGS RESPONSIBLE
WHAT TO DO?
Minor Side Effects (Patient should be encouraged to continue taking medications)
Gastrointestinal intolerance
 Rifampicin
 Give medication at bedtime
Mild skin reactions
 Any kind of drug
 Give antihistamines
Orange/red-colored urine
 Rifampicin
 Reassure the patient
Pain at injection site
 Streptomycin
 Apply warm compress
 Give pyridoxine (Vitamin B6)
Burning sensation in feet
100-200 mg daily for
 IsoniazId
(peripheral neuropathy)
treatment; 10 mg daily for
prevention
 Give aspirin or NSAID
Arthralgia due to hyperuricemia
 Pyrazinamide
 If symptoms persist, consider
gout
Flu-like symptoms (e.g., fever,
 Rifampicin
 Give anti-pyretics
muscle pain)
Major Side Effects (discontinue taking the medications)
Severe skin rash
 Any drug (especially
 Discontinue anti TB drugs &
(hypersensitivity)
streptomycin)
refer
 Discontinue anti TB drugs &
Jaundice due to hepatitis
 Any drug (especially isoniazid,
refer
rifampicin, pyrazinamide)
 If symptoms subside, resume
treatment & monitor clinically
Impairment of visual acuity and
 Discontinue ethambutol &
color vision due to optic
refer to an ophthalmologist
 Ethambutol
neuritis
Hearing impairment, tinnitus
 Discontinue streptomycin &
and dizziness due to damage of
 Streptomycin
refer
CN VIII
Oliguria or albuminuria due to
 Streptomycin
 Discontinue anti TB drugs &
renal disorder
refer
 Rifampicin
Psychosis and convulsion
 Isoniazid
 Discontinue isoniazid & refer
Thrombocytopenia, anemia,
 Rifampicin
 Discontinue anti TB drugs &
shock
refer
D. Treatment Outcomes
OUTCOME
Cured

Treatment completed

Died
Treatment failure



Lost to follow-up
Transfer out


DESCRIPTION
A sputum smear positive patient who has completed treatment and is sputum smear
negative in the last month of treatment and on at least one previous occasion
A patient who has completed treatment, but does not meet the criteria to be
classified as “cured” or “failure”
A patient who dies for any reason during the course of the treatment
Patient who is sputum smear positive at five months o later during treatment
A sputum smear negative patient initially who turned out to be positive during
treatment
Patient whose treatment was interrupted for two consecutive months or more
Patient who has been transferred to another facility with proper referral/transfer slip
for continuation of treatment
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Not evaluated
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A patient for whom no treatment outcome is assigned
Patients transferred to another treatment facility with outcome unknown
PLEURAL EFFUSION
I. ETIOPATHOGENESIS
 Excess quantity of fluid in the pleural space
 Most common cause of pleural effusion is left ventricular failure
 Transudative effusion: occurs when systematic factors that influence the absorption of pleural fluid are altered
 Exudative effusion: occurs when local factors that influence formation and absorption of pleural fluid are altered
II. CLINICAL MANIFESTATIONS
 Patients may present with pleuritic pain, cough and dyspnea
 Findings include decreased breath sounds with decreased or absent tactile fremiti and dullness on percussion
 Tracheal deviation and pleural rub may also be noted
III. DIAGNOSIS AND MANAGEMENT
 First step: determine if effusion is exudative or transudative (use the Light’s criteria by obtaining LDH and protein
level from serum and pleural fluid)
 Other diagnostics for exudative pleural effusions:
o Description of the appearance of the fluid
o Glucose & protein level
o Differential cell count
o Microbiologic studies and cytology
o Work up for tuberculosis
A. Light’s Criteria
Exudative pleural effusions meet at least one of the following criteria:
Pleural fluid protein / serum protein >0.5
Pleural fluid LDH/serum LDH >0.6
Pleural fluid LDH more than two-thirds normal upper limit for serum
These criteria misidentify -25% of transudates as exudates. If one or more of the exudative criteria arte met and the patient is
clinically thought to have a condition producing a transudative effusion, the difference between the protein levels in the serum and
the pleural fluid should be measured. If this gradient >31 g/L, the exudative categorization by these criteria can be ignored because
almost all such patients have transudative pleural effusion
B. Common causes of pleural effusion
Transudative Pleural Effusions
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Effusion due to Heart Failure
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Cirrhosis
Other Transudative Effusions
Exudative Pleural Efusions
Parapneumonic Effusion
Bacterial Pneumonia
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Most common cause of pleural effusion
Diagnostic thoracentesis should be performed:
o If effusions are not bilateral and comparable in
size
o If patient is febrile
o If patient has pleuritic chest pain, to verify that
the patient has a transudative effusion;
otherwise, the heart failure is treated
Pleural fluid N-terminal pro-brain natriuretic peptide
(NT-proBNP) >1500 pg/mL is virtually diagnostic
Liver cirrhosis may give rise to pleural effusion
Usually on the right side (passage of fluid from
abdomen through diaphragm)
Nephritic syndrome, myxedema, urinothorax
Pulmonary embolism (may also be exudative)
Most common cause of exudative pleural effusion
(in the US)
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Lung Abscess
Bronchiectasis
Empyema
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Effusion secondary to Malignancy
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Effusion secondary to Pulmonary Embolism
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Tuberculosis Pleuritis
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Hemothorax
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Presents with acute febrile illness consisting of
chest pain, sputum production and leukocytosis
If free fluid separates the lung from the chest wall
by >10mm, a therapeutic thoracentesis should be
performed
The following factors indicate the need for a more
invasive procedure (e.g., CTT insertion)
o Loculated pleural fluid
o Pleural fluid pH <7.20
o Pleural fluid glucose <3.3 mmol/L (<60mg/dL)
o Positive gram stain or culture of the pleural fluid
o Presence of gross pus in the pleural space
If fluid recurs, a repeat thoracentesis should be
performed
If fluid cannot be completely removed, consider
CTT insertion and instilling fibrinolytics or
performing thoracoscopy to break own adhesions
If
above
procedures
remain
ineffective,
decortications should be considered
Three most common causes: lung CA, breast CA
and lymphoma
Diagnosis usually clinched by cytologic exam of
fluid  if negative, thoracoscopy is the next best
procedure
Glucose levels may be low if tumor burden is high
Patients with malignant effusions are treated
symptomatically for the most part
If patient’s QOL is compromised by dyspnea,
pleurodesis or insertion of a small indwelling
catheter may be considered
Diagnosis most commonly overlooked in the
differential diagnosis of a patient with undiagnosed
pleural effusion
Diagnosis is established by spiral CT scan or
pulmonary arteriography
If the pleural effusion increases in size after
anticoagulation,
consider
recurrent
emboli,
hemothorax or a pleural infection
Most common cause of an exudative pleural
effusion in most parts of the world
Usually associated with primary TB and thought to
be primarily due to a hypersensitivity reaction to TB
protein in pleural space
Cytology shows predominantly small lymphocytes
Diagnosis is established by high levels of
adenosine deaminase (>40 IU/L) or interferon
gamma (>140 pg/mL) in the pleural fluid
Treatment of pleural TB is identical to PTB
Hematocrit should be obtained on pleural fluid if
initial tap reveals bloody pleural fluid
If hematocrit is more than ½ of that in peripheral
blood, hemothorax should be considered and tube
thoracostomy should be inserted
If pleural hemorrhage >200 mL/h, consider
thoracoscopy or thoracotomy
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PNEUMOTHORAX (PTX)
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Presence of gas in the pleural space
I. ETIOPATHOGENESIS
TYPE

Primary Spontaneous
PTX
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Secondary PTX
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Traumatic PTX
Tension PTX
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ETIOLOGY/PATHOGENESIS
Occurs in the absence of underlying
lung disease
Usually due to rupture of apical pleural
blebs
Occurs almost exclusively in smokers
(those with subclinical disease)
Occurs in the presence of underlying
lung disease
Mostly due to COPD (but have been
reported in all lung disease)
Penetrating or non-penetrating chest
injuries
Iatrogenic PTX is a subtype which is
increasingly becoming more common
MANAGEMENT
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Simple aspiration: initial treatment
If lung does not expand or PTX
recurs, thoracoscopic stapling of
blebs and pleural abrasion
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Tube thoracostomy or thoracoscopy
or thoracotomy with bleb stapling
and plural abrasion
If
patient
refuses
surgery,
pleurodesis is an option
Tube thoracostomy unless very small
and
can
be
managed
with
supplemental oxygen or aspiration
If hemopneumothorax: two chest
tubes directed at each lesion
Medical emergency
Large-bore
needle
should
be
inserted into the pleural space
through the 2nd anterior ICS and
should be left in place until a
thoracostomy tube can be inserted
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Pressure in the pleural
SUPERIOR VENA CAVA (SVC) SYNDROME
I. ETIOPATHOGENESIS
 Clinical manifestation of superior vena caval obstruction with severe reduction in venous return from the heart,
neck and upper extremities
 Most common etiologies are lung CA, lymphoma and metastatic tumors
o Lung CA (small cell and squamous cell) accounts for 85% of all cases of malignant origin
 The increasing use of intravascular devices has led to increasing prevalence of benign causes of SVC
 Other benign causes: aneursyms, thyromegaly, thrombosis, fibrosing mediastinitis, histoplasmosis or Behcet’s
syndrome
II. CLINICAL MANIFESTATIONS
 SVCs usually present with neck and facial swelling (especially around the eyes), dyspnea and cough
 Other symptoms are hoarseness, tongue swelling, headaches, nasal congestion, epistaxis, hemoptysis,
dysphagia, pain, dizziness, syncope and lethargy which are aggravated by bending forward or lying down
 PE findings include dilated neck veins, increased number of collateral veins over the anterior chest wall, cyanosis
and edema of the face, arms and chest
 More severe cases present with proptosis, glossal and laryngeal edema, obtundation and signs of cerebral
edema
 Cardiorespiratory symptoms may occur at rest when significant airway and vascular obstruction occurs
 Rarely, esophageal varices may develop
III. DIAGNOSIS OF SVC SYNDROME
DIAGNOSTICS
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Most significant finding is widening of the superior mediastinum (more
commonly on the right side)
Pleural effusion occurs in 25% (often on the right side) - majority are
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Chest CT
Chest MRI
Invasive Procedures
(e.g., broncoscopy, percutaneous
core needle biopsy, mediastinoscopy
and thoracotomy)
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exudative and occasionally chylous
May be normal in some cases
Provides the most reliable view of the mediastinal anatomy
Diminished or absent opacification of central venous structure with
prominent collateral venous circulation
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Necessary for etiologic diagnosis / histologic diagnosis
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IV. MANAGEMENT
 Upper airway obstruction demands emergent therapy:
o Diuretics with low salt diet