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Chen Ring, MD Department Of Respiratory Medicine, The first Affiliated Hospital, University of Zhengzhou
- Bronchiectasis is an abnormal and permanent dilatation of bronchi. - It may be either focal, involving airways supplying a limited region of pulmonary parenchyma, or diffuse, involving airways in a more widespread distribution.
Etiology and Pathogenesis
Congenital bronchiectasis a rare condition in which the lung periphery fails to develop, resulting in cystic dilation of developed bronchi. - Acquired bronchiectasis
Etiology and Pathogenesis
acquired bronchiectasis results from ① direct bronchial wall destruction ， due to - infection - inhalation of noxious chemicals - immunologic reactions - vascular abnormalities that interfere with bronchial nutrition
Bacterial endotoxins and proteases; proteases derived from circulating or pulmonary inflammatory cells; superoxide radicals; and antigen-antibody complexes may mediate bronchial wall damage.
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.
Conditions commonly leading to bronchiectasis
① 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
Conditions commonly leading to bronchiectasis
② bronchial obstruction from any cause-foreign body, enlarged lymph nodes, mucus inspissation, lung cancer
- exposure to a toxic substance that incites a severe inflammatory response. - Examples include inhalation of a toxic gas such as ammonia or aspiration of acidic gastric contents.
ETIOLOGY AND PATHOGENESIS primary ciliary dyskinesia
- responsible for 5 to 10% of bronchiectasis - the primary disorders associated with ciliary dysfunction - the clinical effects include: recurrent upper and lower respiratory tract infections, such as sinusitis, otitis media, and bronchiectasis.
- ½ of patients fall into the subgroup of primary ciliary dyskinesia (PCD) syndromes---Kartagener's syndrome ,in which situs inversus accompanies bronchiectasis and sinusitis.
- may be unilateral or bilateral - most common in the lower lobes, although the right middle lobe and lingular portion of the left upper lobe are often affected.
The bronchial dilatation of bronchiectasis is associated with destructive and inflammatory changes in the walls of medium-sized airways, often at the level of segmental or subsegmental bronchi.
The normal structural components of the wall, may be replaced by fibrous tissue The dilated airways frequently contain pools of thick, purulent material more peripheral airways are often occluded by secretions or obliterated and replaced by fibrous tissue
Additional microscopic features include ：
- bronchial and peribronchial inflammation and fibrosis - ulceration of the bronchial wall - squamous metaplasia - mucous gland hyperplasia.
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.
As a result of the inflammation
- vascularity of the bronchial wall increases, with associated enlargement of the bronchial arteries - anastomoses between the bronchial and pulmonary arterial circulations.
Extensive anastomoses between the bronchial and pulmonary arteries increased blood flow, right-to-left shunts, and hypoxemia lead to pulmonary hypertension and cor pulmonale late in the disease.
Three different patterns of bronchiectasis
In cylindrical bronchiectasis In varicose bronchiectasis In saccular (cystic) bronchiectasis.
In cylindrical bronchiectasis
- the bronchi appear as uniformly dilated tubes that end abruptly at the point that smaller airways are obstructed by secretions
In varicose bronchiectasis
- the affected bronchi have an irregular or beaded pattern of dilatation resembling varicose veins
In saccular (cystic) bronchiectasis
- the bronchi have a ballooned appearance at the periphery, ending in blind sacs without recognizable bronchial structures distal to the sacs.
However, these distinctions have little clinical value, and current pathologic correlations with high-resolution and helical CT characteristics are making this classification obsolete.
CLINICAL MANIFESTATIONS persistent or recurrent cough
purulent sputum production.
(may separate into three layers: frothy at the top, greenish and turbid in the middle, and thick with pus at the bottom.)
Hemoptysis. Dyspnea or wheezing
crackles, rhonchi, and wheezes hypoxemia, may have associated cor pulmonale and right ventricular failure.
Physical findings are nonspecific but persistent crackles over any part of the lungs suggest bronchiectasis. Signs of airflow obstruction tend to be more pronounced in smokers than in nonsmokers. Finger clubbing sometimes occurs with extensive disease and persistent chronic infection
RADIOGRAPHIC AND LABORATORY FINDINGS
the chest radiograph is important ,but often nonspecific: - dilated airways are often crowded together in parallel appearing as "tram tracks“ - when seen in cross-section, they produce "ring shadows."
High-resolution CT (HRCT)
- HRCT (1- to 2-mm cuts) has largely replaced bronchography. - provides an excellent view of dilated airways as seen in cross-sectional images. - the better resolution of HRCT provides results comparable or preferable to bronchography.
Characteristic CT findings
- dilated airways indicated
by tram lines by a signet ring appearance or by grapelike clusters in more severely affected areas.
- thickening of the bronchial walls, obstruction of airways and, sometimes, consolidation seen
a signet ring appearance with a luminal diameter > 1.5 times that of the adjacent vessel in cross section,
Pulmonary function tests
may demonstrate airflow obstruction as a consequence of diffuse bronchiectasis or associated chronic obstructive lung disease.
Examination of sputum
often reveals an abundance of neutrophils and colonization or infection with a variety of possible organisms. Appropriate staining and culturing of sputum often provide a guide to antibiotic therapy.
TREATMENT four major goals
-elimination of an identifiable underlying problem
- improved clearance of tracheobronchial secretions - control of infection - reversal of airflow obstruction
empiric coverage (e.g., with ampicillin, amoxicillin, or cefaclor) is often given initially. quinolone or parenteral therapy with an aminoglycoside or third-generation cephalosporin
- to improve obstruction - and aid clearance of secretions - are particularly useful in patients with airway hyperreactivity and reversible airflow obstruction.
resection or bronchial arterial embolization long-term supplemental oxygen. lung transplantation
defined as necrosis of the pulmonary tissue and formation of cavities containing necrotic debris or fluid caused by microbial infection.
classified based on the duration - acute abscesses :< 4-6 weeks
- chronic abscesses: being of longer duration
classified based on the likely etiology - primary abscess
- secondary abscess
Most frequently, the lung abscess arises as a complication of aspiration pneumonia caused by mouth anaerobes. Other mechanisms for lung abscess formation include bacteremia or tricuspid valve endocarditis, caused by septic emboli to the lung.
anaerobes up to 90%
Peptostreptococcus, Bacteroides, Fusobacterium species, and microaerophilic streptococcus.
other organisms 10%
Staphylococcus aureus, Streptococcus pyogenes Streptococcus pneumoniae (rarely), Klebsiella pneumoniae, and gram-negative bacilli.
History Symptoms depend on whether the abscess is caused by anaerobic or other bacterial infection.
Patients often present with indolent symptoms that evolve over a period of weeks to months. The usual symptoms are fever, cough with sputum production, night sweats, anorexia, and weight loss. The expectorated sputum characteristically is foul smelling and bad tasting. Patients may develop hemoptysis or pleurisy.
These patients generally present with conditions that are more emergent in nature and are usually treated while they have bacterial pneumonia. Cavitation occurs subsequently as parenchymal necrosis ensues. Abscesses from fungi, Nocardia, and mycobacteria tend to have an indolent course and gradually progressive symptoms.
low-grade fever in anaerobic infections
temperatures higher than 38.5°C in other infections. generally, evidence of gingival disease is present consolidation may be present evidence of pleural friction rub , pleural effusion, empyema, and pyopneumothorax may be present. Digital clubbing may develop rapidly.
white blood cell count may reveal leukocytosis and a left shift. Obtain sputum for Gram stain, culture, and sensitivity. If tuberculosis is suspected, AFB&culture is requested. Blood culture may be helpful in establishing the etiology.
A typical appearance -an irregularly shaped cavity with an air-fluid level inside. aspiration Lung abscesses
-frequently occur in the posterior segments of the upper
lobes or the superior segments of the lower lobes.
the cavity wall
-being smooth or ragged but less commonly nodular, which raises the possibility of cavitating carcinoma.
lung necrosis and abscess formation
A lateral chest radiograph shows air-fluid level characteristic of lung abscess
very useful in identification of concomitant empyema or lung infarction. often showning a rounded radiolucent lesion with a thick wall and ill-defined irregular margins.
CT scan shows a thin-walled cavity with surrounding consolidation.
Antibiotic therapy -standard treatment of an anaerobic lung infection is
clindamycin (600 mg IV q8h followed by 150-300 mg PO qid). -shown to be superior over parenteral penicillin in published trials. Several anaerobes may produce beta-lactamase (eg, various species of Bacteroides and Fusobacterium) and therefore develop resistance to penicillin.
Although metronidazole is an effective drug against anaerobic bacteria, the experience with metronidazole in treating lung abscess has been rather disappointing because these infections are generally polymicrobial. A failure rate of 50% has been reported
In hospitalized patients who have aspirated and developed a lung abscess, antibiotic therapy should include coverage against S aureus and Enterobacter and Pseudomonas species.
Duration of therapy
generally for 4-6 weeks. current recommendations
- should continued until the chest radiograph has shown either the resolution of lung abscess or the presence of a small stable lesion.
the rationale for extended treat - risk of relapse exists with a shorter antibiotic regimen.
Response to therapy
Usually show clinical improvement, with improvement of fever, within 3-4 days after initiating the antibiotic therapy. Defervescence is expected in 7-10 days. Persistent fever beyond this time indicates therapeutic failure, and these patients should undergo further diagnostic studies to determine the cause of failure.
Response to therapy
Large cavity size (ie, >6 cm in diameter) usually requires prolonged therapy.
Surgery is very rarely required for patients with uncomplicated lung abscesses. The usual indications for surgery are failure to respond to medical management, suspected neoplasm, or congenital lung malformation. The surgical procedure performed is either lobectomy or pneumonectomy.