DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17

MEDICINE III- PULMONOLOGY JEVAI M.D.

ACUTE RESPIRATORY DISTRESS SYNDROME

Dra. Sta. Maria Exudative
 Damage to alveolar capillary endothelial cells and
type I pneumocytes leakiness to fluid and
macromolecules
 Accumulation of protein rich alveolar and
interstitial fluids (cytokines, lipid mediators)
stiff lungs shunt
 Neutrophilic infiltration
 Vascular obliteration by microthrombi and
fibrocellular infiltration dead space
 Lasts about seven days

Alveolar ch anges in ARDS

Diagnostic Criteria

Clinical Course and Pathophysiology

3 Phases
 Exudative
 Proliferative
 Fibrotic
DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

 Proliferative
 Progressive lung injury
 Early pulmonary fibrosis
 Lasts from day 7 – 21 days of illness
 Shift to a lymphocyte-predominant pulmonary
infiltrate
 Proliferation of Type II pneumocyte along alveolar
basement membranes
 Alveolar type III procollagen peptide – marker of
pulmonary fibrosis with a protracted clinical
course and increased mortality
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

 Fibrotic
 Initiation of ductal and interstitial fibrosis leading
to emphysema-like changes
 Intimal proliferation pulmonary hypertension
 Increased mortality

Clinical Characteristics
 tachypnea - earliest sign dyspnea
 low pO 2, low PCO2
 fine rales
 CXR clear or few scattered infiltrates
 cyanosis, dyspneic
 prominent rales
 extensive infiltrates
 intractable hypoxemia

Treatment
General Principles
 Treat underlying medical and surgical disorder
 Minimize procedures and their complications
 Deep venous thrombosis prophylaxis, stress gastritis, CVP
catheter infections
 Treat nosocomial infection
 Provide adequate nutrition

Management of Mechanical Ventilation

 Ventilator induced lung injury
 Alveolar overdistention
 Recommend low tidal vol 5 ml/kg
 Alveolar collapse
 reduced lung compliance (stiff lungs)
 optimal PEEP (12 – 15 ) to minimize
FiO2 and maximize PaO2
 inverse ration ventilation (I:E >1:1)
 prone position

Low VT in ARDS
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

 DIC
 Functional recovery within 6 months from ARDS

ECMO in ARDS

Table 258-1
Major
Etiologies of
Bronchiectasis
and Proposed
Workup

Pattern of Etiology by Categories (with Workup

Management of Mechanical Ventilation Lung Specific Examples)
 Fluid management – maintain low left atrial filling pressure Involvement by
 Glucocorticoids Bronchiectasis
 Other therapies
 Surfactant replacement therapy Inhaled nitric oxide Focal Obstruction (e.g., aspirated Chest imaging (chest
foreign body, tumor mass) x-ray and/or chest
Factors increasing mortality CT); bronchoscopy
 Advanced age
 >75 years old (60% mortality), < 45 years old (20% Diffuse Infection (e.g., bacterial, Gram's stain/culture;
mortality) nontuberculous stains/cultures for
 Sepsis mycobacterial) acid-fast bacilli and
 Sepsis + age >60 (mortality 3X higher) fungi. If no pathogen
 Preexisting organ dysfunction from chronic illness is identified, consider
 Chronic liver disease, cirrhosis, alcohol abuse, bronchoscopy with
chronic immunosuppression, sepsis, chronic renal bronchoalveolar
failure, increased APACHE scores lavage (B AL)
 Higher mortality in ARDS due to direct lung trauma
Immunodeficiency (e.g., Complete blood count
Comp lications hypogammaglobulinemia, with differential;
 oxygen toxicity HIV infection, bronchiolitis immunoglobulin
 barotrauma obliterans after lung measurement; HIV
 nosocomial pneumonia transplantation) testing
 bronchopleural fistula
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION
MEDICINE III- PULMONOLOGY
Genetic causes (e.g., cystic
fibrosis, Kartagener's
syndrome, 1 antitrypsin
deficiency)
Autoimmune or
rheumatologic causes (e.g.,
rheumatoid arthritis,
Sjögren's syndrome,
inflammatory bowel
disease); immune-mediated
disease (e.g., allergic
bronchopulmonary
aspergillosis)
Recurrent aspiration
Miscellaneous (e.g., yellow
nail syndrome; traction
bronchiectasis from
postradiation fibrosis or
idiopathic pulmonary
fibrosis)
Idiopathic
a
Skin testing for
Aspergillus
reactivity;
measurement of
serum
precipitins for
Aspergillus,
serum IgE
levels, serum
eosinophils, etc.
KRENOVIANTZ ’17
JEVAI M.D.
Measurement of Table 258-2 Microbial Path ogen s Causing Cavitary Lung
chloride levels in Infection
sweat (for cystic
fibrosis), 1 antitrypsin
levels; nasal or
respiratory tract
brush/biopsy (for Aspiration-Prone Host
dyskinetic/immotile
cilia syndrome);
genetic testing Anaerobic bacteria plus microaerophilic and/or anaerobic
streptococci, Gemella spp.
Clinical examination
with careful joint Embolic (endovascular) lesions: usually Staphylococcus aureus,
exam, serologic testing Pseudomonas aeruginosa, Fusobacterium necrophorum a
(e.g., for rheumatoid
factor). Consider
workup for allergic
bronchopulmonary Endemic fungi: Histoplasma, Blastomyces, Coccidioides spp.
aspergillosis,
especially in patients
with refractory Mycobacteria: M. tuberculosis, M. kansasii, M. avium
asthma a
Test of swallowing Immunocompromised Host
function and general
neuromuscular
M. tuberculosis, Nocardia asteroides, Rhodococcus eq ui,
strength
Legionella spp., P. aeruginosa, Enterobacteriaceae (especially
Klebsiella pneumoniae), Aspergillu s spp., Cryptococcus spp.
Guided by clinical
condition
Previously Healthy Host
Bacteria: S. aureus, bS. milleri, K. pneumoniae, group A
Streptococcus; Gemella, Legionella, and Actinomyces spp.
Exclusion of other
causes
Parasites: Entamoeba histolytica, Paragonimus westermani,
Strongyloides stercoralis
a
Lemierre's disease.
b
Often in a young patien t with influenza.
RESPIRATORY FAILURE
Types of respiratory failure
 Type I, Acute Hypoxemic Respiratory Failure
 alveolar flooding and subsequent intrapulmonary
shunt physiology occur.
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION
MEDICINE III- PULMONOLOGY
 consequence of pulmonary edema, pneumonia, or
alveolar hemorrhage.
 Pulmonary edema can be further categorized
 elevated pulmonary microvascular
pressures as seen in heart failure
 intravascular volume overload or ARDS
("low-pressure pulmonary edema
Type II Resp iratory Failu re
 alveolar hypoventilation and results in the inability to
eliminate carbon dioxide effectively.
 Mechanisms:
 impaired central nervous system (CNS) drive to
breathe
 drug overdose, brainstem injury, sleep-
disordered breathing, and
hypothyroidism.
 impaired strength with failure of neuromuscular
function in the respiratory system
 impaired neuromuscular transmission
(e.g., myasthenia gravis, Guillain-Barré
syndrom e, amyotrophic lateral sclerosis,
phrenic nerve injury) or respiratory
muscle weakness (e.g., myopathy,
electrolyte derangements, fatigue
 increased load(s) on the respiratory system.
 subclassified into
 increased resistive loads
(bronchospasm)
 reduced lung compliance
[alveolar edema, atelectasis,
intrinsic positive end-
expiratory pressure (autoPEEP)
 loads due to reduced chest wall
compliance (pneumothorax,
pleural effusion, abdominal
distention)
 increased minute ventilation
requirements (Pulmonary
embolus with increased dead
space fraction, sepsis).
Type III Respiratory Failure
 result of lung atelectasis
 also called perioperative respiratory failure.
 general anesthesia decreases functional residual capacity lead
to collapse of dependent lung units.
Type IV Resp iratory Failu re
 results from hypoperfusion of respiratory muscles in patients
in shock.
 Normally, respiratory muscles consume <5% of the total
cardiac output and O2 delivery.
Pulmonary Edema
KRENOVIANTZ ’17
JEVAI M.D.
Diagnosis
 rapid onset of dyspnea at rest, tachypnea, tachycardia, and
severe hypoxemia.
 Rales and wheezing due to airway compression from
peribronchial cuffing may be audible.
 Hypertension is usually present due to release of endogenous
catecholamines.
 difficult to distinguish between cardiogenic and
noncardiogenic
 Echocardiography may identify
ventricular dysfunction and valvular lesions.
 ECG - ST elevation and evolving Q waves of
acute MI
 Brain natriuretic peptide levels
 Swan-Ganz catheter to measure PCWP
Treatment
 Support the circulation, gas exchange, and lung mechanics.
 Correct infection, acidemia, anemia, and renal failure
 Support of Oxygenation and Ventilation
 LV failure (arrhythmia, ischemia/infarction)
responds to O2 therapy
 noncardiogenic edema require mechanical
ventilation.
 Oxygen Therapy
 Positive-Pressure Ventilation
 Noninvasive ventilation
 Mechanical ventilation with PEEP
 (1) decreases both preload and
afterload, thereby improving
cardiac function
 (2) redistributes lung water
from the intraalveolar to the
extraalveolar space
 (3) increases lung volume to
avoid atelectasis.
 Reduction of Preload
 Diuretics ("loop diuretics" furosemide, bum etanide,
and torsemide)
 Nitrates (Nitroglycerin and isosorbide dinitrate)
 Sublingual nitroglycerin (0.4 mg x 3
every 5 min)
 IV nitroglycerin, commencing at 5–10
g/min.
 IV nitroprusside (0.1–5 g/kg per min)
 Reduction of Preload
 Morphine 2- to 4-mg IV boluses
 Angiotensin-Converting Enzyme (ACE) Inhibitors
reduce both afterload and preload
 Other Preload-Reducing Agents
 IV recombinant brain natriuretic peptide
(nesiritide)
 Physical Methods
 sitting position with the legs dangling
along the side of the bed.
 Inotropic and Inodilator Drugs
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

 The sympathomimetic amines dopamine reserved for refractory patients and is not recommended in
and dobutamine the setting of ischemia or MI.
 Digitalis Glycosides - inotropes  Physical Methods
 Intraaortic Counterpulsation  Reduction of venous return reduces preload. Patients without
 Other causes hypotension should be maintained in the sitting position with
 Iatrogenic cardiogenic shock the legs dangling along the side of the bed.
 Acute STEMI complicated by pulmonary edema is  Inotropic and Inodilator Drugs
associated with in-hospital mortality rates of 20–  The sympathomimetic amines dopamine and dobutamine
40%. (see above) are potent inotropic agents. The bipyridine
 Reexpansion pulmonary edema phosphodiesterase-3 inhibitors (inodilators), such as
 High-altitude pulmonary edema milrinone (50 g/kg followed by 0.25–0.75 g/kg per min),
 dexamethasone, calcium channel- stimulate myocardial contractility while promoting
blocking drugs, or long-acting inhaled 2- peripheral and pulmonary vasodilation. Such agents are
adrenergic agonists. indicated in patients with cardiogenic pulmonary edema and
 descent from altitude, bed rest, oxygen, severe LV dysfunction.
and, if feasible, inhaled nitric oxide
 For pulmonary edema resulting from upper airway
 of hypoalbuminemia, hyponatremia, or hypochloremia.
Furosem ide is also a venodilator that reduces preload rapidly,
before any diuresis, and is the diuretic of choice. The initial
dose of furosemide should be 0.5 mg/kg, but a higher dose (1
mg/kg) is required in patients with renal insufficiency,
chronic diuretic use, or hypervolemia or after failure of a
lower dose.
 Nitrates
 Nitroglycerin and isosorbide dinitrate act predominantly as
venodilators but have coronary vasodilating properties as
well. They are rapid in onset and effective when
administered by a variety of routes. Sublingual nitroglycerin
(0.4 mg x 3 every 5 min) is first-line therapy for acute
cardiogenic pulmonary edema. If pulmonary edema persists
in the absence of hypotension, sublingual may be followed Causes of Respiratory Failure
by IV nitroglycerin, commencing at 5–10 g/min. IV
nitroprusside (0.1–5 g/kg per min) is a potent venous and
arterial vasodilator. It is useful for patients with pulmonary
edema and hypertension but is not recommended in states of
reduced coronary artery perfusion. It requires close
monitoring and titration using an arterial catheter for
continuous BP measurement.
 Morphine
 Given in 2- to 4-mg IV boluses, morphine is a transient
venodilator that reduces preload while relieving dyspnea and
anxiety. These effects can diminish stress, catecholamine
levels, tachycardia, and ventricular afterload in patients with
pulmonary edema and systemic hypertension.
 Angiotensin-Converting Enzyme (ACE) Inhibitors
 ACE inhibitors reduce both afterload and preload and are
recommended for hypertensive patients. A low dose of a
short-acting agent may be initiated and followed by
Chron ic Ventilatory Disorder
increasing oral doses. In acute MI with heart failure, ACE
inhibitors reduce short- and long-term mortality rates.
 reflected in abnormal PaCO 2
 Other Preload-Reducing Agents
 PaCO2 = (k)(V.CO2)/V. A,
 IV recombinant brain natriuretic peptide (nesiritide) is a
 where V. CO2 carbon dioxide production
potent vasodilator with diuretic properties and is effective in
 k is a constant
the treatment of cardiogenic pulmonary edema. It should be
 V. A is fresh gas alveolar ventilation
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MEDICINE III- PULMONOLOGY
 PaCO2 levels depend:
 CO2 production
 minute ventilation
 dead space fraction.
 The spontaneous cycle of inspiration and expiration is
automatically generated in the brainstem.
 medulla
 the dorsal respiratory group (DRG)
 ventral respiratory column (VRC).
 These neurons have widespread
projections, including the descending
projections into the contralateral spinal
cord, where they perform many
functions.
Hypoventilation
Diseases that reduce minute ventilation or increase dead space
Four major categories:
 parenchymal lung and chest wall disease
 sleep disordered breathing
 neuromuscular disease
 respiratory drive disorders
 Signs and Symptoms of Hypoventilation
 Dyspnea during activities of daily living
 Orthopnea in diseases affecting diaphragm
function
 Poor quality sleep
 Daytime hypersomnolence
 Early morning headaches
 Anxiety
 Impaired cough in neuromuscular diseases
 Clinical course
 An asymptomatic stage where daytime PaO2 and
PaCO2 are normal,
 nocturnal hypoventilation, initially during rapid
eye movement (R EM) sleep and later in non-REM
sleep.
 If vital capacity drops further, daytime hypercapnia
develops.
 the hallmark of all alveolar hypoventilation
syndrom es is an increase in alveolar PCO2
(PACO2) and, therefore, in PaCO2.
 respiratory acidosis --- compensatory increase in
plasma bicarbonate concentration.
 erythrocytosis.
 induce pulmonary vasoconstriction, pulmonary
hypertension, right-ventricular hypertrophy, and
right heart failure.
Diagnosis
 ABG - elevated PaCO2 with a normal pH, elevated plasma
bicarbonate
 Physical examination, imaging studies (chest x-ray and/or
CT scan), and pulmonary function tests are sufficient to
KRENOVIANTZ ’17
JEVAI M.D.
identify most lung/chest wall disorders leading to
hypercapnia.
 screen for obstructive sleep apnea (OSA)
 If the ventilatory apparatus (lung, airways, chest wall) is
intact, suspect respiratory drive and neuromuscular disorders.
 increase in minute ventilation in response to elevated CO2
and/or low O2 – do sleep study
 Brain imaging (CT scan or MRI) - structural abnormalities in
the pons or medulla
 Chronic narcotic use, hypothyroidism
 Respiratory muscle weakness
Treatment:
 Nocturnal noninvasive positive-pressure ventilation (NIPPV)
improve daytime hypercapnia, prolong survival, and improve
health-related quality of life when daytime hypercapnia is
documented.
ALS guidelines recommend nocturnal NIPPV
 Paco2 45 mmHg
 nocturnal oximetry demonstrates oxygen saturation
88% for 5 consecutive minutes
 maximal inspiratory pressure <60 cm H2O; and
FVC <50% predicted. nocturnal, but not daytime,
hypercapnia
Treat the underlying disorder.
 medroxyprogesterone and acetazolamide
 supplemental oxygen is effective in attenuating hypoxemia,
polycythemia, and pulmonary hypertension.
 Phrenic nerve or diaphragm pacing for high cervical spinal
cord lesions or respiratory drive disorders.
Hypoventilation Syndromes
 Obesity Hypoventilation Syndrome
 body mass index (B MI) 30 kg/m2
 sleep-disordered breathing and chronic
daytime alveolar hypoventilation,
defined as PaCO2 45 mmHg, and PaO2 <
70 mmHg in the absence of other known
causes of hypercapnia.
 obstructive sleep apnea syndrome,
defined by an apnea hypopnea index 5
AND daytime sleepiness, is
approximately 3–4% in middle-aged men
and 2% in middle-aged women.
DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

 Symptoms:dyspnea, paresthesias, tetany, headache, dizziness,

visual disturbances, and atypical chest pain.
 often misattributed by the patient and health care workers to
cardiopulmonary disorders
 anxiety disorders and panic attacks are NOT synonymous
with hyperventilation.
 Exclude systemic illnesses such as diabetic ketoacidosis.
 A high index of suspicion is required as increased minute
ventilation can be difficult to detect on physical examination.
(sigh, yawn 2 – 3X/minute

Treatment:
 few well-controlled treatment studies.
 reassurance and frank discussion
 Identifying and eliminating habits that perpetuate hypocapnia
(yawning or sigh breathing)
 breathing exercises and diaphragmatic retraining may be
Treatment: beneficial for some patients.
 weight reduction  Beta-blockers (sym pathetically mediated symptoms)
 continuous positive airway pressure (C PAP) therapy during
sleep Once neural input has been delivered to the respiratory pump muscles,
normal gas exchange requires an adequate amount of respiratory
muscle strength to overcome the elastic and resistive loads of the
respiratory system (F ig. 264-1A, Chap. 252). In health, the strength of
the respiratory muscles readily accomplishes this, and normal
respiration continues indefinitely.

 The spontaneous cycle of inspiration and expiration is

automatically generated in the brainstem.
 medulla
 the dorsal respiratory group (DRG)
 ventral respiratory column (VRC). These
neurons have widespread projections,
including the descending projections into
the contralateral spinal cord, where they
perform many functions.

Hypoventilation
Central Hypoventilation Syndrome
 shortness of breath and diminished exercise tolerance.
 Ondine's curse or congenital central hypoventilation
 Episodes of increased dyspnea and sputum production are
syndrom e (C CHS).
hallmarks of obstructive lung diseases, such as chronic
 Abnormalities in the gene encoding PHOX2b, a transcription
obstructive pulmonary disease (C OPD)
factor with a role in neuronal development
 whereas progressive dyspnea and cough are common in
 have absent respiratory response to hypoxia or hypercapnia,
interstitial lung diseases. Excessive daytime somnolence,
mildly elevated PaCO2 while awake, and markedly elevated
poor quality sleep, and snoring are common among patients
PaCO2 during non-REM sleep.
with sleep-disordered breathing. Sleep disturbance and
 Compensate V E to "normalize" PaCO2 during exercise.
orthopnea are also described in neuromuscular disorders.
 Treatment
 NIP PV
 mechanical ventilation
 phrenic nerve or diaphragmatic pacing at centers
with experience performing these procedures.

Hyperventilation
 ventilation in excess of metabolic requirements (CO2
production) leading to a reduction in PaCO2
DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

Mallampati Grading
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

BRONCHIECTASIS

 Irreversible airway dilatation of bronchi

◦ Focal
◦ diffuse
 Pathology:
◦ destruction and inflammation in the walls of
medium-sized airways (segmental and
subsegm ental bronchi) followed by fibrosis
◦ micros:bronchial and peribronchial inflammation,
fibrosis, ulceration of bronchial wall, squamous
metaplasia, mucus gland hypertrophy
◦ increased bronchial wall vascularity

Etiology and Path ogen esis

 Vicious cycle hypothesis Clinical Man ifestations
◦ Infectious: cycle of inflammation - impaired  recurrent cough
clearance-infection  purulent phlegm
 Pseudomonas, Haemophilus  hemoptysis
 measles, pertussis, adenovirus, influenza  dyspnea
 Staph, Klbesiella, TB  PE rales, rhonchi,wheeze, clubbing, RV failure
 Impaired host defense and endobronchial
obstruction
◦ Non-infectious causes
◦ following inhalation of Ammonia or aspiration of
gastric contents
a 1 - antitrypsin deficiency

Pathogenesis

Clubbing

 Rad iographic and Laboratory Findings

◦ Normal in mild disease
◦ “tram tracks ”, signet ring shadows on CXR
◦ CTscan
◦ Bronchography
◦ Sputum exam + bacterial growth
◦ PFT: airflow obstruction with partial reversibility

 Reid ’s Classification
Bronchograp hy
DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

Table 258-1
Major
Etiologies of
Bronchiectasis
and Proposed
Workup

Pattern of Etiology by Categories (with Workup

Lung Specific Examples)
Involvement by
Bronchiectasis

Focal Obstruction (e.g., aspirated Chest imaging (chest

foreign body, tumor mass) x-ray and/or chest
CT); bronchoscopy

Diffuse Infection (e.g., bacterial, Gram's stain/culture;

nontuberculous stains/cultures for
mycobacterial) acid-fast bacilli and
fungi. If no pathogen
is identified, consider
bronchoscopy with
bronchoalveolar
lavage (B AL)

Immunodeficiency (e.g., Complete blood count

hypogammaglobulinemia, with differential;
HIV infection, bronchiolitis immunoglobulin
obliterans after lung measurement; HIV
transplantation) testing
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION
MEDICINE III- PULMONOLOGY
Genetic causes (e.g., cystic
fibrosis, Kartagener's
syndrome, 1 antitrypsin
deficiency)
Autoimmune or
rheumatologic causes (e.g.,
rheumatoid arthritis,
Sjögren's syndrome,
inflammatory bowel
disease); immune-mediated
disease (e.g., allergic
bronchopulmonary
aspergillosis)
Recurrent aspiration
Miscellaneous (e.g., yellow
nail syndrome; traction
bronchiectasis from
postradiation fibrosis or
idiopathic pulmonary
fibrosis)
Idiopathic
a
Skin testing for
Aspergillus
reactivity;
measurement of
serum
precipitins for
Aspergillus,
serum IgE
levels, serum
eosinophils, etc.
KRENOVIANTZ ’17
JEVAI M.D.
Measurement of
chloride levels in
sweat (for cystic
fibrosis), 1 antitrypsin
levels; nasal or Table 258-2 Microbial Path ogen s Causing Cavitary Lung
respiratory tract Infection
brush/biopsy (for
dyskinetic/immotile
cilia syndrome);
genetic testing
Aspiration-Prone Host
Clinical examination
with careful joint
exam, serologic testing Anaerobic bacteria plus microaerophilic and/or anaerobic
(e.g., for rheumatoid streptococci, Gemella spp.
factor). Consider
workup for allergic
bronchopulmonary Embolic (endovascular) lesions: usually Staphylococcus aureus,
aspergillosis, Pseudomonas aeruginosa, Fusobacterium necrophorum a
especially in patients
with refractory
asthma a
Endemic fungi: Histoplasma, Blastomyces, Coccidioides spp.
Test of swallowing
function and general
neuromuscular
Mycobacteria: M. tuberculosis, M. kansasii, M. avium
strength
Guided by clinical Immunocompromised Host
condition
M. tuberculosis, Nocardia asteroides, Rhodococcus eq ui,
Legionella spp., P. aeruginosa, Enterobacteriaceae (especially
Klebsiella pneumoniae), Aspergillu s spp., Cryptococcus spp.
Exclusion of other
causes
Previously Healthy Host
Bacteria: S. aureus, bS. milleri, K. pneumoniae, group A
Streptococcus; Gemella, Legionella, and Actinomyces spp.
Parasites: Entamoeba histolytica, Paragonimus westermani,
Strongyloides stercoralis
a
Lemierre's disease.
b
Often in a young patien t with influenza.
 DOÑA REMEDIOS TRINIDAD ROMUALDEZ MEDICAL FOUNDATION KRENOVIANTZ ’17
MEDICINE III- PULMONOLOGY JEVAI M.D.

Treatment
 Eliminate identifiable problem
 Bronchial hygiene - chest PT
 Control infection -antibiotics
 reverse airflow obstruction - bronchodilators
 Bronchial artery embolization, resection, transplant

Comp lications:
 Recurrent infection
 hemoptysis

Prognosis:
 - repeated infection leands to decline in FEV 1 50 – 55
ml/year