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MEDICINE III- PULMONOLOGY

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

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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

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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

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DIC
Functional recovery within 6 months from ARDS

ECMO in ARDS

Table 258-1
Major
Etiologies of
Bronchiectasis
and Proposed
Workup

Management of Mechanical Ventilation


Fluid management maintain low left atrial filling pressure
Glucocorticoids
Other therapies
Surfactant replacement therapy Inhaled nitric oxide
Factors increasing mortality
Advanced age
>75 years old (60% mortality), < 45 years old (20%
mortality)
Sepsis
Sepsis + age >60 (mortality 3X higher)
Preexisting organ dysfunction from chronic illness
Chronic liver disease, cirrhosis, alcohol abuse,
chronic immunosuppression, sepsis, chronic renal
failure, increased APACHE scores
Higher mortality in ARDS due to direct lung trauma
Comp lications
oxygen toxicity
barotrauma
nosocomial pneumonia
bronchopleural fistula

Pattern of
Etiology by Categories (with Workup
Lung
Specific Examples)
Involvement by
Bronchiectasis
Focal

Obstruction (e.g., aspirated


foreign body, tumor mass)

Chest imaging (chest


x-ray and/or chest
CT); bronchoscopy

Diffuse

Infection (e.g., bacterial,


nontuberculous
mycobacterial)

Gram's stain/culture;
stains/cultures for
acid-fast bacilli and
fungi. If no pathogen
is identified, consider
bronchoscopy with
bronchoalveolar
lavage (B AL)

Immunodeficiency (e.g.,
hypogammaglobulinemia,
HIV infection, bronchiolitis
obliterans after lung
transplantation)

Complete blood count


with differential;
immunoglobulin
measurement; HIV
testing

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MEDICINE III- PULMONOLOGY
Genetic causes (e.g., cystic
fibrosis, Kartagener's
syndrome, 1 antitrypsin
deficiency)

Skin testing for


Aspergillus
reactivity;
measurement of
serum
precipitins for
Aspergillus,
serum IgE
levels, serum
eosinophils, etc.

Measurement of
chloride levels in
sweat (for cystic
fibrosis), 1 antitrypsin
levels; nasal or
respiratory tract
brush/biopsy (for
dyskinetic/immotile
cilia syndrome);
genetic testing

Autoimmune or
rheumatologic causes (e.g.,
rheumatoid arthritis,
Sjgren's syndrome,
inflammatory bowel
disease); immune-mediated
disease (e.g., allergic
bronchopulmonary
aspergillosis)

Clinical examination
with careful joint
exam, serologic testing
(e.g., for rheumatoid
factor). Consider
workup for allergic
bronchopulmonary
aspergillosis,
especially in patients
with refractory
asthma a

Recurrent aspiration

Test of swallowing
function and general
neuromuscular
strength

Miscellaneous (e.g., yellow


nail syndrome; traction
bronchiectasis from
postradiation fibrosis or
idiopathic pulmonary
fibrosis)

Guided by clinical
condition

Idiopathic

Exclusion of other
causes

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Table 258-2 Microbial Path ogen s Causing Cavitary Lung


Infection

Aspiration-Prone Host

Anaerobic bacteria plus microaerophilic and/or anaerobic


streptococci, Gemella spp.
Embolic (endovascular) lesions: usually Staphylococcus aureus,
Pseudomonas aeruginosa, Fusobacterium necrophorum a

Endemic fungi: Histoplasma, Blastomyces, Coccidioides spp.

Mycobacteria: M. tuberculosis, M. kansasii, M. avium

Immunocompromised Host

M. tuberculosis, Nocardia asteroides, Rhodococcus eq ui,


Legionella spp., P. aeruginosa, Enterobacteriaceae (especially
Klebsiella pneumoniae), Aspergillu s spp., Cryptococcus spp.

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

Lemierre's disease.
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.

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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, sleepdisordered breathing, and
hypothyroidism.
impaired strength with failure of neuromuscular
function in the respiratory system
impaired neuromuscular transmission
(e.g., myasthenia gravis, Guillain-Barr
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 endexpiratory 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

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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 510
g/min.
IV nitroprusside (0.15 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

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MEDICINE III- PULMONOLOGY

The sympathomimetic amines dopamine


and dobutamine
Digitalis Glycosides - inotropes
Intraaortic Counterpulsation
Other causes
Iatrogenic cardiogenic shock
Acute STEMI complicated by pulmonary edema is
associated with in-hospital mortality rates of 20
40%.
Reexpansion pulmonary edema
High-altitude pulmonary edema
dexamethasone, calcium channelblocking drugs, or long-acting inhaled 2adrenergic agonists.
descent from altitude, bed rest, oxygen,
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
by IV nitroglycerin, commencing at 510 g/min. IV
nitroprusside (0.15 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
increasing oral doses. In acute MI with heart failure, ACE
inhibitors reduce short- and long-term mortality rates.
Other Preload-Reducing Agents
IV recombinant brain natriuretic peptide (nesiritide) is a
potent vasodilator with diuretic properties and is effective in
the treatment of cardiogenic pulmonary edema. It should be

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reserved for refractory patients and is not recommended in


the setting of ischemia or MI.
Physical Methods
Reduction of venous return reduces preload. Patients without
hypotension should be maintained in the sitting position with
the legs dangling along the side of the bed.
Inotropic and Inodilator Drugs
The sympathomimetic amines dopamine and dobutamine
(see above) are potent inotropic agents. The bipyridine
phosphodiesterase-3 inhibitors (inodilators), such as
milrinone (50 g/kg followed by 0.250.75 g/kg per min),
stimulate myocardial contractility while promoting
peripheral and pulmonary vasodilation. Such agents are
indicated in patients with cardiogenic pulmonary edema and
severe LV dysfunction.

Causes of Respiratory Failure

Chron ic Ventilatory Disorder

reflected in abnormal PaCO 2


PaCO2 = (k)(V.CO2)/V. A,
where V. CO2 carbon dioxide production
k is a constant
V. A is fresh gas alveolar ventilation

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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

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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.

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

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 34% in middle-aged men
and 2% in middle-aged women.

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Treatment:
weight reduction
continuous positive airway pressure (C PAP) therapy during
sleep

Hyperventilation
ventilation in excess of metabolic requirements (CO2
production) leading to a reduction in PaCO2

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
beneficial for some patients.
Beta-blockers (sym pathetically mediated symptoms)
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.

Central Hypoventilation Syndrome


Ondine's curse or congenital central hypoventilation
syndrom e (C CHS).
Abnormalities in the gene encoding PHOX2b, a transcription
factor with a role in neuronal development
have absent respiratory response to hypoxia or hypercapnia,
mildly elevated PaCO2 while awake, and markedly elevated
PaCO2 during non-REM sleep.
Compensate V E to "normalize" PaCO2 during exercise.
Treatment
NIP PV
mechanical ventilation
phrenic nerve or diaphragmatic pacing at centers
with experience performing these procedures.

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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
shortness of breath and diminished exercise tolerance.
Episodes of increased dyspnea and sputum production are
hallmarks of obstructive lung diseases, such as chronic
obstructive pulmonary disease (C OPD)
whereas progressive dyspnea and cough are common in
interstitial lung diseases. Excessive daytime somnolence,
poor quality sleep, and snoring are common among patients
with sleep-disordered breathing. Sleep disturbance and
orthopnea are also described in neuromuscular disorders.

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Mallampati Grading

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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

Infectious: cycle of inflammation - impaired


clearance-infection

Pseudomonas, Haemophilus

measles, pertussis, adenovirus, influenza

Staph, Klbesiella, TB

Impaired host defense and endobronchial


obstruction

Non-infectious causes

following inhalation of Ammonia or aspiration of


gastric contents
a 1 - antitrypsin deficiency

Clinical Man ifestations


recurrent cough
purulent phlegm
hemoptysis
dyspnea
PE rales, rhonchi,wheeze, clubbing, RV failure

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

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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


foreign body, tumor mass)

Chest imaging (chest


x-ray and/or chest
CT); bronchoscopy

Diffuse

Infection (e.g., bacterial,


nontuberculous
mycobacterial)

Gram's stain/culture;
stains/cultures for
acid-fast bacilli and
fungi. If no pathogen
is identified, consider
bronchoscopy with
bronchoalveolar
lavage (B AL)

Immunodeficiency (e.g.,
hypogammaglobulinemia,
HIV infection, bronchiolitis
obliterans after lung
transplantation)

Complete blood count


with differential;
immunoglobulin
measurement; HIV
testing

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MEDICINE III- PULMONOLOGY
Genetic causes (e.g., cystic
fibrosis, Kartagener's
syndrome, 1 antitrypsin
deficiency)

Measurement of
chloride levels in
sweat (for cystic
fibrosis), 1 antitrypsin
levels; nasal or
respiratory tract
brush/biopsy (for
dyskinetic/immotile
cilia syndrome);
genetic testing

Autoimmune or
rheumatologic causes (e.g.,
rheumatoid arthritis,
Sjgren's syndrome,
inflammatory bowel
disease); immune-mediated
disease (e.g., allergic
bronchopulmonary
aspergillosis)

Clinical examination
with careful joint
exam, serologic testing
(e.g., for rheumatoid
factor). Consider
workup for allergic
bronchopulmonary
aspergillosis,
especially in patients
with refractory
asthma a

Recurrent aspiration

Test of swallowing
function and general
neuromuscular
strength

Miscellaneous (e.g., yellow


nail syndrome; traction
bronchiectasis from
postradiation fibrosis or
idiopathic pulmonary
fibrosis)

Guided by clinical
condition

Idiopathic

Exclusion of other
causes

KRENOVIANTZ 17
JEVAI M.D.

Table 258-2 Microbial Path ogen s Causing Cavitary Lung


Infection

Aspiration-Prone Host

Anaerobic bacteria plus microaerophilic and/or anaerobic


streptococci, Gemella spp.
Embolic (endovascular) lesions: usually Staphylococcus aureus,
Pseudomonas aeruginosa, Fusobacterium necrophorum a

Endemic fungi: Histoplasma, Blastomyces, Coccidioides spp.

Mycobacteria: M. tuberculosis, M. kansasii, M. avium

Immunocompromised Host

M. tuberculosis, Nocardia asteroides, Rhodococcus eq ui,


Legionella spp., P. aeruginosa, Enterobacteriaceae (especially
Klebsiella pneumoniae), Aspergillu s spp., Cryptococcus spp.

Previously Healthy Host


a

Skin testing for


Aspergillus
reactivity;
measurement of
serum
precipitins for
Aspergillus,
serum IgE
levels, serum
eosinophils, etc.

Bacteria: S. aureus, bS. milleri, K. pneumoniae, group A


Streptococcus; Gemella, Legionella, and Actinomyces spp.

Parasites: Entamoeba histolytica, Paragonimus westermani,


Strongyloides stercoralis

Lemierre's disease.
Often in a young patien t with influenza.

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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

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