THE KURSK STATE MEDICAL UNIVERSITY
DEPARTMENT OF SURGICAL DISEASES № 1
BRONCHIECTASIS
Information for self-training of English-speaking students
The chair of surgical diseases N 1 (Chair-head - prof. S.V.Ivanov)
BY ASS. PROFESSOR I.S. IVANOV
KURSK-2010
Bronchiectasis
Bronchiectasis: Irreversible focal bronchial dilation, usually accompanied by
chronic infection and associated with diverse conditions, some congenital or
hereditary.
Bronchiectasis may be focal and limited to a single segment or lobe of the lung, or
it may be widespread and affect multiple lobes in one or both lungs.
Etiology and Pathogenesis
Congenital bronchiectasis is a rare condition in which the lung periphery fails to
develop,
resulting
in
cystic dilation
of
developed
bronchi.
Acquired
bronchiectasis results from (1) direct bronchial wall destruction--due to infection,
inhalation of noxious chemicals, immunologic reactions, or vascular abnormalities
that interfere with bronchial nutrition--or (2) mechanical alterations--due to
atelectasis or loss of parenchymal volume with increased traction on the walls of
airways, leading to bronchial dilation and secondary infection. Bacterial
endotoxins and proteases; proteases derived from circulating or pulmonary
inflammatory cells; superoxide radicals; and antigen-antibody complexes may
mediate bronchial wall damage. Amounts of functionally active neutrophil
elastase, cathepsin G, and neutrophil matrix metalloproteinase MMP-8 found in
bronchoalveolar lavage fluid increase with the severity of disease in moderate to
severe
bronchiectasis.
Furthermore,
the
antiproteases
1-antitrypsin
and
antichymotrypsin may be proteolytically or oxidatively cleaved into lower
molecular weight forms, which provide less protection against enzymatic
destruction of extracellular matrix. Detection of proinflammatory cytokines
interleukin-1 (IL-1 ), IL-8, and tumor necrosis factor-alpha in sputum and
demonstration of chemokine and cytokine bronchial cell interactions have led to
the hypothesis that such interactions may result in recruitment and activation of
certain inflammatory cells, affect their survival, and modulate ongoing
inflammation, a cardinal feature of bronchiectasis. Nitric oxide, which affects the
immune response, cell signaling, and plasma exudation at inflammatory sites, may
help perpetuate the inflammatory response in bronchiectasis. Exhaled nitric oxide
is increased in patients with bronchiectasis compared with normal subjects and
bronchiectatic patients taking inhaled corticosteroids.
Conditions commonly leading to bronchiectasis are severe pneumonia (especially
when complicating measles, pertussis, or certain adenovirus infections in children);
necrotizing pulmonary infections due to Klebsiella sp, staphylococci, influenza
virus, fungi, mycobacteria, and, rarely, mycoplasmas; and bronchial obstruction
from any cause (eg, foreign body, enlarged lymph nodes, mucus inspissation, lung
cancer, or other lung tumor). Miscellaneous chronic fibrosing lung diseases (eg,
those following aspiration pneumonia or inhalation of injurious gases or particles-eg, silica, talc, or bakelite) also predispose to bronchiectasis. Immunologic
deficiencies, including AIDS, and various other acquired, congenital, and
hereditary abnormalities that increase host susceptibility to infection or impair
respiratory defenses are less common but important predisposing factors. Although
incidence and mortality have decreased with the widespread use of antibiotics and
immunizations in children, bronchiectasis as a manifestation of cystic fibrosis is
still common. (Cystic fibrosis (mucoviscidosis; fibrocystic disease of the pancreas;
pancreatic cystic fibrosis): An inherited disease of the exocrine glands, primarily
affecting the GI and respiratory systems, and usually characterized by COPD,
exocrine pancreatic insufficiency, and abnormally high sweat electrolytes).
Bronchiectasis, along with situs inversus and sinusitis, is a feature of Kartagener's
syndrome, a subgroup of the primary ciliary dyskinesia (PCD) syndromes. In
these syndromes, structural or functional abnormalities in ciliary organelles result
in defective mucociliary clearance that leads to suppurative bronchial infections
and bronchiectasis as well as chronic rhinitis, serous otitis media, male sterility,
corneal abnormalities, sinus headaches, and a poor sense of smell. Bronchiectasis
can occur in patients with Young syndrome, which is characterized by obstructive
azoospermia, chronic sinopulmonary infections, normal spermatogenesis, a dilated
epididymal head filled with spermatozoa, and amorphous material without
spermatozoa in the region of the corpus. Absent are the ciliary abnormalities seen
in the PCD syndromes, the genetic and electrolyte abnormalities characteristic of
cystic fibrosis, and the genetic mutations found in congenital absence of the vas
deferens, which accounts for about 6% of obstructive azoospermia.
An unusual pattern of bronchiectasis occurs in allergic bronchopulmonary mycosis
(An allergic reaction to Aspergillus fumigatus occurring in asthmatic patients as
eosinophilic pneumonia): The proximal bronchi are dilated rather than the
medium-sized subsegmental or peripheral bronchi as in idiopathic bronchiectasis.
Bronchial wall damage is thought to be due to an immunologic response to a
colonizing protease-producing fungus, most commonly Aspergillus fumigatus,
permitting the organism to persist and inflammation and destruction to continue.
The reported association of bronchiectasis with probable or possible autoimmune
diseases, such as rheumatoid arthritis, Sjögren's syndrome, Hashimoto's thyroiditis,
and ulcerative colitis, has not been satisfactorily explained.
Pathophysiology
Bronchiectasis may be unilateral or bilateral; it is most common in the lower lobes,
although the right middle lobe and lingular portion of the left upper lobe are often
affected. The traditional classification as cylindrical, varicose, or saccular is based
on the pathologic and bronchographic appearance. However, these distinctions
have little clinical value, and current pathologic correlations with high-resolution
and helical CT characteristics are making this classification obsolete.
Pathologically, bronchial walls show extensive inflammatory destruction, chronic
inflammation, increased mucus, and loss of cilia. Where adjacent interstitial and
alveolar areas are destroyed, tissue reorganization and fibrosis result in loss of
volume. Bronchiectasis is generally associated with chronic bronchitis and/or
emphysema and some fibrosis.
The extent and character of the pathologic changes determine the functional and
hemodynamic abnormalities, which often include reduced lung volumes and
airflow rates, ventilation/perfusion defects, and hypoxemia. Extensive anastomoses
between the bronchial and pulmonary arteries may occur, with marked
enlargement of bronchial arteries. Anastomoses between bronchial and pulmonary
veins also enlarge. The resultant increased blood flow, right-to-left shunts, and
hypoxemia lead to pulmonary hypertension and cor pulmonale late in the disease.
CLASSIFICATION
1. unilateral, bilateral, total damage.
2. cylindrical,saccular and mixed bronhiectasis
3. anatomic localization (nomber of the lobe, etc)
4. with or without complications
CLINICO-ANATOMICAL CLASSIFICATION
1.the first stage – cylindrical bronhiectasis, are localized in basal segments of
lungs, unilateral damage. Tretment – conservative.
2.the second stage – cylindrical and saccular bronhiectasis, unilateral damage.
Treatment – conservative and surgical treatment (segmentectomy, lobectomy,
pulmonectomy- if there are no contraindications)
3/the third stage – saccular, bilateral bronhiectasis. Symptomatic conservative
treatment.
Symptoms and Signs
Bronchiectasis, which can develop at any age, begins most often in early
childhood, but symptoms may not be apparent until much later. Their severity and
characteristics vary widely from patient to patient and from time to time in an
individual, depending largely on the extent of the disease and the presence and
extent of complicating chronic infection. Most patients have chronic cough and
sputum production--the most characteristic and common symptoms--but
occasionally, a patient is asymptomatic. These symptoms often begin insidiously,
usually after a respiratory infection, and tend to worsen gradually over a period of
years. Severe pneumonia with incomplete clearing of symptoms and residual
persistent cough and sputum production is a common mode of onset. As the
condition progresses, the cough tends to become more productive. Typically, it
occurs regularly in the morning on arising, late in the afternoon, and on retiring;
many patients are relatively free of cough during the intervening hours. Sputum
usually is similar to that of bronchitis and is not characteristic. Less commonly, in
long-standing cases, sputum is abundant and may separate into three layers: frothy
at the top, greenish and turbid in the middle, and thick with pus at the bottom.
Hemoptysis from erosion of capillaries, but sometimes from anastomoses between
the bronchial and pulmonary arterial systems, is common and may be the first and
only complaint. Recurrent fever or pleuritic pain, with or without visible
pneumonia, is also common; investigation of such symptoms may lead to the
diagnosis of bronchiectasis. Wheezing, shortness of breath and other
manifestations of respiratory insufficiency, and cor pulmonale (Heart failure
(congestive heart failure): Symptomatic myocardial dysfunction resulting in a
characteristic pattern of hemodynamic, renal, and neurohormonal responses) may
occur in advanced cases with associated chronic bronchitis and emphysema.
Physical findings are nonspecific, but persistent crackles over any part of the lungs
suggest bronchiectasis. Signs of airflow obstruction (decreased breath sounds,
prolonged expiration, or wheezing) tend to be more pronounced in smokers than in
nonsmokers. Finger clubbing sometimes occurs with extensive disease and
persistent chronic infection (Measuring finger clubbing. The ratio of the
anteroposterior diameter of the finger at the nail bed (a-b) to that at the distal
interphalangeal joint (c-d) is a simple measurement of finger clubbing. It can be
obtained readily and reproducibly with calipers. If the ratio is > 1, clubbing is
present. Clubbing is also characterized by loss of the normal angle at the nail bed).
Diagnosis
Bronchiectasis must be suspected in anyone with the above symptoms and signs.
Standard chest x-rays may show increased bronchovascular markings from
peribronchial fibrosis and intrabronchial secretions, crowding from an atelectatic
lung, tram lines (parallel lines outlining dilated bronchi due to peribronchial
inflammation and fibrosis), areas of honeycombing, or cystic areas with or without
fluid levels, but occasionally x-rays are normal. High-resolution CT (HRCT) of the
chest (1- to 2-mm cuts) has largely replaced bronchography. With 10-mm
collimation, dilation of small bronchi may be missed, but the better resolution of
HRCT provides results comparable or preferable to bronchography. Its widespread
use indicates that bronchiectasis is probably more common than can be diagnosed
by clinical findings and standard x-rays alone.
Characteristic CT findings are dilated airways, indicated by tram lines, by a signet
ring appearance with a luminal diameter > 1.5 times that of the adjacent vessel in
cross section, or by grapelike clusters in more severely affected areas. These
dilated medium-sized bronchi may extend almost to the pleura because of the
destruction of lung parenchyma. Thickening of the bronchial walls, obstruction of
airways (evidenced by opacification--eg, from a mucus plug--or by air trapping),
and, sometimes, consolidation are other findings.
Helical CT may be considered for surgical candidates because at least one study
has shown it to be superior to HRCT in identifying the extent of bronchiectasis and
distribution within a given segment, but the additional radiation exposure has
prevented it from supplanting HRCT for general use. HRCT may be performed
with or without contrast; the precise protocol is tailored to the patient's clinical
situation. Excessive secretions or blood in the bronchial tree or acute
bronchopneumonia can lead to misinterpretation. The reversible dilation that
occurs with airspace consolidation (eg, pneumonia) should not be confused with
true bronchiectasis. Chronic bronchitis often accompanies and may mimic
bronchiectasis, but recurrent hemoptysis, fever, and pleuritic pain and the x-ray
abnormalities help distinguish bronchiectasis from chronic bronchitis alone.
Mycobacterial and fungal infections should be ruled out, because they are
treatable. Sputum cultures, bronchial washings, serologic studies for fungal antigen
or antibodies, and even biopsy of appropriate tissue (but not highly vascular
bronchiectatic airways) may be indicated. When CT reveals multiple small nodules
with bronchiectasis in a nonimmunocompromised host without cystic fibrosis,
Mycobacterium avium-intracellulare complex (MAIC) cultures are commonly
positive, and in some patients, MAIC granulomas suggest disease rather than mere
colonization.
When disease is unilateral or of recent onset, fiberoptic bronchoscopy is indicated
to rule out tumor, foreign body, or other localized endobronchial abnormality.
HRCT is often performed first to provide maximum information to the
bronchoscopist in advance, but bronchoscopy is usually still necessary for precise
pathologic diagnosis.
Associated conditions should be sought, particularly cystic fibrosis, immune
deficiencies, and predisposing congenital abnormalities. Such a search is most
important in symptomatic younger patients and in patients with particularly severe
or frequently recurring infections. Cystic fibrosis should be suspected if the
abnormalities on x-ray occur predominantly in the apices or upper lobes.
Pancreatic insufficiency is a feature in children but is not common in adults, in
whom pulmonary manifestations predominate. Diagnosis of cystic fibrosis is based
on sweat test results (Cystic fibrosis (mucoviscidosis; fibrocystic disease of the
pancreas; pancreatic cystic fibrosis): An inherited disease of the exocrine glands,
primarily affecting the GI and respiratory systems, and usually characterized by
COPD,
exocrine
pancreatic
insufficiency,
and
abnormally
high
sweat
electrolytes.). Genetic testing may be informative in fertile patients who have
unexplained bronchiectasis with normal pancreatic function and sweat electrolytes.
Young syndrome, more common than cystic fibrosis or PCD syndromes, should be
suspected in men with chronic recurrent sinopulmonary symptoms and infertility.
Normal spermatozoa, testicular function, and sweat test results distinguish it from
typical cystic fibrosis or PCD syndromes. Some patients with vas deferens
abnormality have mutations in the cystic fibrosis gene, but such mutations have not
yet been demonstrated in those with Young syndrome.
PCD syndromes occur in 11% of children with chronic respiratory disease.
Diagnosis is confirmed by examining the ultrastructure and function (motility, beat
frequency) of nasal or other respiratory cilia, obtained via biopsy or brushing, and
by measuring nasal ciliary clearance time--the time it takes for a patient to first
taste saccharin after it is instilled above the inferior turbinate of the nose (normal:
12 to 15 min). Interpreting ciliary abnormalities involves excluding nonspecific
ciliary defects, which can be present in <= 10% of cilia in patients with acquired
pulmonary disease and in healthy persons; recognizing that infection can cause
transient dyskinesia; and being aware that ciliary characteristics of patients and
healthy persons can overlap. Ciliary ultrastructure may be normal in patients with
PCD syndromes, perhaps because of biochemical and molecular abnormalities that
affect function but not ultrastructure.
Immunoglobulin (Ig) deficiencies may be identified by serum Ig measurements. If
serum protein electrophoresis detects low -globulin levels, serum IgG, IgA, and
IgM should be measured. Even when total levels of IgG or IgA are normal, some
IgG subclass deficiencies have been associated with sinopulmonary infections; IgG
subclasses should be measured in patients with unexplained bronchiectasis.
1-
Antitrypsin ( 1-antiprotease inhibitor) deficiency, which is occasionally associated
with bronchiectasis, may be suspected when
1-globulin
is low and may be
confirmed by phenotyping with crossed immunoelectrophoresis.
Congenital abnormalities of tracheal or bronchial cartilage and connective tissue
are usually detected on x-ray. In tracheobronchomegaly (Mounier-Kuhn
syndrome), the trachea is about twice as wide as normal. In the rare WilliamsCampbell syndrome, total or partial absence of cartilage beyond the main
segmental
bronchi
produces
wheezing
and
dyspnea early in
infancy;
bronchoscopy, CT, or newer imaging techniques may show inspiratory ballooning
and expiratory collapse of the affected bronchi. The yellow nail syndrome,
believed to be due to a congenital hypoplasia of the lymphatic system, is
recognized by thickened, curved, yellowish to greenish nails and primary
lymphedema. Some patients have exudative pleural effusion and bronchiectasis.
Allergic bronchopulmonary aspergillosis may be suspected when there is a wheal
and flare reaction to fungal antigens, serum IgE is high, serum precipitins for
Aspergillus fumigatus or another fungus are elevated, and the clinical picture
suggests it. Blood and sputum eosinophilia are often present.
Prophylaxis
Awareness and early identification of conditions frequently associated with
bronchiectasis may permit earlier therapy that may prevent its development or
reduce its severity. More than half the cases of pediatric bronchiectasis can be
accurately diagnosed and promptly managed to lessen morbidity. When there is a
family history of cystic fibrosis, prenatal diagnosis by DNA analysis to identify
specific mutations may permit very early treatment and guide counseling.
Childhood immunization against pertussis and measles, widespread use of
antibiotics, and improved living conditions and nutrition have helped reduce the
prevalence, morbidity, and mortality of bronchiectasis. Influenza vaccine yearly
and pneumococcal vaccine one time (or repeated after 6 yr for persons at particular
risk and likely to respond) may be helpful and are increasing in clinical
importance. Early treatment of respiratory syncytial virus infection with ribavirin
aerosol and prompt treatment of pneumonia may lessen their damaging potential.
Appropriate treatment of pneumonia is based on the age of the patient, presence of
comorbidities, severity of the infection, probable source, and likely pathogens.
Ig replacement in deficiency states, early detection and removal of foreign bodies
and localized bronchial obstructions, treatment of recurrent sinusitis, and
prevention and prompt treatment of conditions predisposing to aspiration of
infected or toxic material may prevent repeated chest infections or damage that
leads to bronchiectasis. Ig replacement, reported to reduce the number and severity
of chest infections in Ig deficiency states, may be especially beneficial in patients
with a documented impairment in antibody production after a specific challenge.
Immune globulin is given IM in doses sufficient to maintain an infection-free state.
IV immune globulin (IVIG) is also available. Trough levels of serum IgG > 500
mg/dL are associated with fewer infections and better pulmonary function than are
lower levels. IVIG may do more than passively supply antibody. It may neutralize
some bacteria-derived toxins or otherwise supplement host anti-inflammatory
defenses. Dose and frequency must be tailored to the patient. Inhalation of noxious
gases and particulates, including cigarette smoke, should be avoided or minimized
by using effective environmental controls or personal protective devices. When
acute inhalation injury occurs, prompt treatment of complicating infection and
judicious use of a corticosteroid may reduce inflammatory damage.
Treatment
Treatment is directed against infections, secretions, airway obstruction, and
complications (eg, hemoptysis, hypoxemia, respiratory failure, cor pulmonale).
Treatment of infection includes antibiotics, bronchodilators, and physical therapy
to promote bronchial drainage. Sputum usually contains gram-positive and gramnegative microorganisms (eg, Streptococcus pneumoniae, Haemophilus influenzae,
Staphylococcus aureus, Moraxella [Branhamella] catarrhalis, Pseudomonas sp);
anaerobes commonly inhabit bronchiectatic cysts. A broad-spectrum antibiotic (eg,
ampicillin 250 to 500 mg po q 6 h for adults or 50 to 100 mg/kg/day in divided
doses q 6 to 8 h for children, with a maximum dose of 2 to 3 g/day for large
children; amoxicillin 250 to 500 mg po q 8 h for adults or 40 mg/kg/day in divided
doses for children; or, only for adults, tetracycline 250 to 500 mg po q 6 h) is often
used until the sputum is nonpurulent and less voluminous, about 1 to 2 wk.
Trimethoprim-sulfamethoxazole (TMP-SMX) 320/1600 mg po q 12 h for 14 days
can also reduce sputum volume and eliminate pathogens; for children, TMP-SMX
6/30 to 12/60 mg/kg/day is given in divided doses q 12 h, depending on the size of
the child and severity of the infection. Tetracycline or trimethoprim can inhibit
increased airway absorption of sodium in vitro and might have a double benefit in
a disease such as cystic fibrosis, in which enhanced sodium absorption in the
airways is believed to contribute to inspissated secretions. A newer macrolide, such
as clarithromycin or azithromycin, or a 2nd-generation cephalosporin is another
possible choice. Antibiotics should be repeated at the first sign of recurring
infection (eg, increased volume or purulence of sputum). If infection recurs often,
prolonged chemoprophylaxis with ampicillin, amoxicillin, or tetracycline may be
tried but is generally disappointing. In severe cases, high-dose amoxicillin (3 g po
bid) is reported to achieve higher serum and sputum concentrations than do equal
doses of ampicillin.
Prophylactic or suppressive antimicrobial regimens can reduce the bacterial load
(associated with purulence and destructive elastase activity in some), but there is
no consensus about long-term continuous versus intermittent therapy or about
specific regimens. With short-term therapy (1 to 2 wk), purulence and elastase
activity rapidly return to pretreatment levels. One goal is to prevent development
of resistant microorganisms and conditions favoring Pseudomonas sp, which is
particularly difficult to eradicate. Regimens include an oral antibiotic for 7 to 10
days each mo, 7 to 10 days of treatment alternating with equal rest periods,
continuous long-term treatment with a reduced dose, or high doses of an antibiotic
(such as amoxicillin) for 3 to 6 mo. A fluoroquinolone, such as ciprofloxacin 500
to 750 mg po bid, may be effective and can be given long-term, but resistance
frequently develops after one or two treatment cycles. In severe cases, aerosol or
IV regimens may be needed, but resistance is always a problem. Alternating drugs
may help avoid early resistance and persistence of pneumococci, which tends to
occur with ciprofloxacin.
For bronchopneumonia or serious respiratory infection, parenteral antibiotics-chosen on the basis of Gram stain, cultures, and sensitivity studies--are indicated.
Cefuroxime 750 mg IV tid for 48 to 72 h followed by cefuroxime axetil 500 mg po
bid for 5 days is as effective as amoxicillin 1.2 g IV tid with clavulanic acid
followed by amoxicillin 625 mg po tid. Amoxicillin penetrates lung secretions,
especially in the presence of active inflammation, but some local inactivation may
occur, correlating with
-lactamase levels. For broader coverage to include
Mycoplasma, Legionella, and Pseudomonas sp, a macrolide plus a 3rd-generation
cephalosporin (such as ceftazidime or cefoperazone) plus an aminoglycoside can
be used, or piperacillin or azlocillin with an aminoglycoside can be used when
Pseudomonas predominates.
When cultures for Mycobacterium tuberculosis are positive, appropriate
antituberculosis treatment is required based on the clinical history and laboratory
findings, but MAIC commonly colonizes the lungs of patients with bronchiectasis,
so treatment is reserved for patients with strongly suspected or proven disease. An
empirical multidrug regimen for MAIC may include clarithromycin 500 mg po bid,
ethambutol 25 mg/kg po daily, clofazimine 200 mg po daily, and streptomycin 10
to 12 mg/kg/day IM or amikacin 12 to 15 mg/kg IM three times a week for 1 to 2
mo, followed by clarithromycin 750 mg po daily, ethambutol 15 mg/kg po daily,
and clofazimine 50 to 100 mg po daily for 3 to 24 mo, usually given until cultures
are negative for 12 mo. Basing therapy on drug susceptibility testing, however, is
important.
Patients with bronchiectasis should avoid cigarette smoke and other irritants and
refrain from using sedatives or antitussives. Postural drainage, clapping, and
vibration performed regularly may facilitate sputum clearance in some patients.
Diffuse chronic bronchitis, often accompanying bronchiectasis, should be treated
accordingly.
2-Agonists,
theophylline, and corticosteroids may decrease airflow
obstruction, facilitate ciliary clearance, and reduce inflammation. If asthma or
allergic bronchopulmonary aspergillosis is also present, corticosteroids may be
especially beneficial in reducing inflammation, and in young children, who are
most susceptible to fungal sensitization, they may enhance fungal elimination.
Itraconazole 200 to 400 mg/day po reduces the corticosteroid requirements,
reduces serum IgE, and improves airflow rates in a small number of patients with
allergic bronchopulmonary aspergillosis, but antifungal drugs are usually reserved
for invasive Aspergillus infection.
Other drugs--such as the mucolytic N-acetylcysteine and recombinant human
deoxyribonuclease (rhDNase), which breaks down DNA in purulent sputum--may
benefit selected patients but have no proven benefit in bronchiectasis. NSAIDs,
such as indomethacin, have been tried experimentally. Despite mild reduction in
sputum volume and changes in peripheral neutrophil function, sputum elastase and
myeloperoxidase levels were not reduced, and viable bacterial load was not altered
in bronchial secretions.
Chronic hypoxemia should be treated with O2, particularly if the PaO2 in a stable
patient is < 55 mm Hg on room air or if there is evidence of pulmonary
hypertension or secondary polycythemia. Respiratory failure and cor pulmonale
should be treated as in other patients with chronic obstructive airway disorders.
Intubation and mechanical ventilation should, if possible, be avoided, because the
ability to cough is lost and the risk of inadequately evacuating secretions by
suctioning alone and of promoting further infection is enhanced. Lung
transplantation can be performed in patients with advanced cystic fibrosis and
bronchiectasis. Double lung transplantation is usually the procedure of choice.
Surgical resection is rarely necessary but should be considered when conservative
management yields to recurrent pneumonia, disabling bronchial infections, or
frequent hemoptysis and the disease is sufficiently localized and stable. For
massive pulmonary hemorrhage, emergency resection or embolization of the
bleeding vessel (usually a bronchial artery) can be lifesaving.