| What is bronchiectasis? | Irreversible airway dilation either focused or diffuse, can be cylindrical or tubular, varicose or cystic
Caused by inflammatory destruction of muscular and elastic component of bronchial wall. |
| How is pathogenesis of bronchiectasis? | 2 factors, insulting agent and impaired drainage, airway obstruction or defect in host defense
Host response of neutrophils secreting proteases, inflammatory cytokines and ROS, create transmural inflammation, mucosal edema, cratering, ulceration and neovascularization of airways
Progressive destruction is due to unopposed NE activity, neutrophils have increased viability, reduced phagocytosis, increased release of myeloperoxidase, and impaired bacterial killing (pseudomonas for example)
Presence of Atopy as well converys worse clinical course in COPD and asthma
CF can contribute to it through dysfunction of airway sodium and chloride channels
Vitamin D deficiency as well increases colonization, inflammation and symptoms |
| What are etiologies causing broncheictasis? | Numerous, identified in 60-90% of cases.
Acquired Bronchial Obstruction, Congenital anatomic defects causing bronchial obstruction, immunodeficiency state, abnormal secretion state, miscellaneous disorders |
| What are etiologies of acquired bronchial obstruction? | Foreign body aspiration, tumors (laryngeal papillomatosis, adenoma, endobronchial teratoma), hilar adenopathy (TB, sarcoidosis), COPD, mucoid impaction (allergic aspergillosis, granulomatosis, post-op), other (polychondritis, tracheobronchial amyloidosis) |
| What are etiologies of congenital anatomic defects causing bronchial obstruction? | Tracheobronchial (bronchomalacia, cyst, cartilage deficiency (william-campbell), tracheobronchomegaly (Mounier-Kuhn), ectopic bronchus, fistula)
Vascular (pulmonary sequestering and aneurysm)
lymphatic (yellow-nail syndrome |
| What are etiologies of immunodeficiency? | IgG def (congenital agammaglobinemia, selective def, acquired def, hypogammaglob (Nezlof / Bare lymphocyte syndrome)
IgA (selective def, Ataxia-Telangiectasia syndrome)
Leukocyte dysfunction (Chronic granulomatous disease -NADPH oxidase dysfunction)
Other rare ones (WHIM, hypergammaglobinemia) |
| What are etiologies of abnormal secretion? | Ciliary defects of mucosa (primary ciliary dyskinesia (w/ or w/out situs inversus - Kartagener syndrome)
CF (early childhood symptoms, later get sinopulmonary symptoms)
Young's syndrome (obstructive azoospermia with sinopulmonary infections) |
| What are etiologies of miscellaneous disease causing broncheictasis? | a1-antitrypsin deficiency, recurrent aspiration pneumonia (alcoholism, neuro disorders), Rheumatic disease (RA, sjogren), IBD (Crhon's), Toxic fume inhalation (amonia, NO2), Chronic rejection following transplant (obliterative bronchiolitis), childhood infections (measles, pertusis), bacterial viral and other infections |
| What are the clinical manifestations of broncheictasis? | Cough and daily production of mucopurulent tenacious sputum lasting months -> years
Less common is dry cough with episodes of hemoptysis, less common is dyspnea wheezing and pleuritic pain.
Usually hx of many infections, but may occur from one infection
On PE: we hear crackles in 75%, wheezing 22% and clubbing only in 2%.
May present with fatigue (43%, lower FEV1), urinary incontienence (47% women), reduced smell |
| What are the radiology findings in broncheictasis? | Linear atelectasis, dilated thickened airways, irregular peripheral opacities (mucopurulent plugs)
CT (airway dilation (>1,5 times normal -> cylindrical bronchiectasis), signet-ring sign (cross-sectioned dilated air filled bronchus contiguous with smaller nodular opacity of pulmonary artery (looks like a ring with a stone), we see lack of tapering in combination with bronchial dilation (since dilation alone maybe asthma)
Tree-in-bud pattern when small airways affected reflect aspiration/ infection persistent.
Cysts seen in severe forms (Cystic bronchiectasis) clustered like grapes |
| How are LFTs in bronchiectasis? | Spirometry before and after bronchodilators, see obstructive impairment (low FEV1, low FEV1/FVC) in advanced disease very low FVC (lung destroyed) |
| What are the common infections in broncheictasis? | Colonizing flora, haemophilus influenza, moraxella catarrhalis, staph aureus, pseudomonas, strep pneumo (more hx of abx -> more resistant), pseudomonas should have earlier anti-pseudomonas agents, and should get IV Abx. |
| What is the treatment course of bronchiectasis? | treat underlying disease (injury/ infection/ immunodef (IVIG/ SCIG)/tracheobronchomegaly (stent in airway), some can be controlled to prevent scarring)
Treat acute exacerbations (infections (more sputum darker color, with other symptoms ans systemic complaints), pneumothorax/ pneumonia )
Oral antibiotic treatment (stable pt)
IV treatment (sputum with pseudomonas (nonquinolone tx of pseudomonas given IV), hospitalization (exacerbations), aminoglycosides (may be nephrotoxic/ ototoxic so monitor it), some are hard to eradicate (aspergillus (central bronchiectasis), Mycobacteria avium MAC) -therapy prednisone 0.5-1 mg'kg for 2 weeks, 16 week anti-fungals)
Prevention of exacerbation
Abx (macrolide usually - chronic low dose)
Airway clearance therapy (directed cough, exercise, forced expiration, chest physical exercise, PEP...)
Others (dilators, anti inflammatory, statin (NSAID), PPI and H2 blockers for GERD complication, pulmonary rehab |
| When is surgery indicated? | Removal of obstructed by tumor part, reduction of infective episodes, overwhelming purulent mucus, risk of hemorrhage, areas with resistant organisms (MAC, TB) |
| How to we manage hemoptysis? | Produced by injury to superficial mucosal neovascular arterioles.
urgent surgery needed for life-threatening one, but most pt can be managed by flexible bronchoscopy and chest CT to localize bleed, and bronchoscopic procedure (argon plasma coagulation, laser, electrocautery, vasoconstrictive agents), if uneffecitve: arteriographic embolization used (preserves lungs and no need for surgery) |
| What are lung abscesses? | Necrosis of parenchyma caused by infection (anaerobes) |
| How are lung abscesses classified? | Primary (prone to aspiration pt or previously healthy ones)
Secondary (with other systemic disease like HIV, transplant...)
They can also be classified according to causative bacteria. |
| How is the pathogenesis of lung abscesses? | Most are complications of aspiration pneumonia (due to reduced conscioussness or dysphagia) with periodontal diseases (gingivitis)
Bacteria aren't cleared due to low consciousness, causes pneumonia first then progresses to tissue necrosis 7-14 days later, result in abscess/ empyema (due to fistula/ extension of infection to pleural space).
May occur in Lemierre's syndrome/ jugular vein thrombophlebitis (begins in pharynx, spreads in neck and goes to jugular vein, causing bacteremia and septic emboli to lungs
Tricuspid valve endocarditis (By staph - can cause septic emboli to both lungs) |
| How is microbiology of lung abscesses? | Polymicrobial usually, anaerobes of gingiva, most common peptostrep, prevotella, bacteroides, fusobacterium. (Strep anginosus most common - monobacterial abscess) |
| How are lung abscesses in immunocompromised pt? | Most common is pseudomonas, mucormycosis, Mycobacterium TB, non TB mycobacteria, rhodococcus. |
| What are the clinical manifestations of lung abscesses? | Most have indolent symptoms evolving over weeks- months.
Fever, cough, sputum, chronic disease (night sweats, weight loss, anemia), hemoptysis, none have chills, sour-tasting sputum. |
| What are PE findings in pt with lung abscesses? | Gingival cervice disease, reduced conscious/ dysphagia, fever, abnormal lung sounds (pleural effusion/ parenchymal disease), Pulmonary infiltrates |
| How is manifestation of SA lung abscesses? | Most common fulminant disease in young adults with underlying influenza.
May be MRSA and have PVL gene, so we have shock, neutropenia, lung necrosis, high mortality (even with Abx treatment)
Risk for getting it in hospitalization, long term, surgery, hemodialysis, other infections, IV drug use, military service |
| How is manifestation of kleb and nocardia? | Kleb: rapid necrosis and slow response to Abx
Nocardia: In immunocompromised particularly. |
| What is the differential dx of lung abscess? | Typically dx by CXR (pulmonary infiltrate, with cavity (necrosis))
May be necrotizing infections, empyema with air-fluid level (hydropneumothorax), septic pulmonary emboli (infectious causes)
Pulmonary embolism, vasculitis, neoplasm, broncheictasis, sarcoidosis, rheumatic nodule, foreign body aspiration (non-infectious causes) |
| What is treatment of lung abscess? | Antimicrobial therapy (empiric, targeted).
Surgery
Response to therapy |
| What are healthcare-associated pneumonias? | HAP, occur 48 hours or more after admission , VAP (develops 48 hours after endotracheal intubation)
Occur due to drug resistance (multidrug resistance (MDR), extensive drug resistance (only sensitive for 1 only) XDR, and Pan drug resistance (PDR) |
| How is epidemiology of HAP? | one of most common infections, occur in non-ventilated pt, but highest risk is ventilated pt.
VAP associated with increased cost and stays (increased it 4 days) |
| How is pathogenesis of HAP? | 45% aspirate in sleep inoculum of bacteria in presence of endotracheal tube depending on number and virulence of organisms
Usually aerobic gram + bacteria, sometimes viruses |
| What are risk factors of MDR VAP? | IV Abx past 90 days, septic shock at time of VAP, ARDS before VAP, >5days before VAP occurring, renal replacement therapy, for MRSِA (unit with 10% MRSA), for pseudomonas (same) |
| How is dx of HAP? | New lung infiltrate, evidence of infection (fever, leukocytosis, oxygen decline, sputum) but no specific dx symptoms, all low sensitivity.
Histology very useful (more than cultures of sputum) |
| How is tx of HAP? | Empiric therapy (against SA, pseudomonas and other gram-bacilli)
For 7 days mostly, severe cases may need longer (empyema, abscesses, metastatic...) |
