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Inflammatory and suppurative diseases of lungs

Inflammatory and suppurative diseases of lungs
Definition: To the pathologist, pneumonia is an infection of the alveoli, distal airways,
and interstitium of the lung that is manifested by increased weight of the lungs, replacement of the normal lung’s sponginess by consolidation, and alveoli filled with white blood cells, red blood cells, and fibrin. To the clinician, pneumonia is a constellation of symptoms and signs (fever, chills, cough, pleuritic chest pain, sputum production, hyper- or hypothermia, increased respiratory rate, dullness to percussion, bronchial breathing, egophony, crackles, wheezes, pleural friction rub) in combination with at least one opacity on chest radiography.
Community-acquired pneumonia remains a common illness.
Approximately 4.5 million cases of community-acquired pneumonia occur annually, and 20% result in hospitalization. Estimates of incidence of nosocomial pneumonia range from 4-7 episodes per 1000 hospitalizations. Approximately 25% of patients in intensive care units (ICUs) develop pneumonia. Overall incidence of community-acquired pneumonia is reported to be 170 cases per 100,000 persons. With advancing age, the incidence increases from 94 cases per 100,000 persons in patients aged 44 years to 280 cases per 100,000 persons in those older than 65 years. Pneumonia as a cause of hospitalization increased from 36 to 48 cases per 100,000 Etiology: The >100 documented microbial causes of pneumonia include bacteria, fungi,
viruses, and parasites. Fortunately, most cases of pneumonia are caused by a few common respiratory pathogens, including S. pneumoniae, H. influenzae, S. aureus, M. pneumoniae, C. pneumoniae, Moraxella catarrhalis, Legionella spp., aerobic gram-negative bacteria, influenza viruses, adenoviruses, and respiratory syncytial virus. Overall, S. pneumoniae accounts for _50% of all cases of pneumonia requiring admission to the hospital, although in everyday practice the etiology of pneumonia is unknown in up to 70% of patients. The past 30 years have seen the identification of new etiologic agents of pneumonia, often during the detailed investigation of dramatic outbreaks. Thus Legionella pneumophila was isolated during the investigation of an outbreak of pneumonia at a convention of the American Legion in Philadelphia in 1976. Other etiologic agents identified during this period include C. pneumoniae, hantavirus, Nipah virus, Hendra virus, and metapneumovirus. Investigations of an outbreak of severe acute respiratory syndrome (SARS) originating in China and Hong Kong during the winter of 2003 and subsequently found to be caused by a novel coronavirus are ongoing.
Pathogenesis: Routes of Infection For pneumonia to occur, a potential pathogen must
reach the lower respiratory tract in sufficient numbers or with sufficient virulence to overwhelm host defenses. Possible routes include gross aspiration, microaspiration, aerosolization, hematogenous spread from a distant infected site, and direct spread from a contiguous infected site. By far the most common route for bacterial pneumonia is microaspiration of oropharyngeal secretions colonized with pathogenic microorganisms. Host Factors Pneumonia is more
common when host defense is impaired, as it is in severe underlying illness.
Hypogammaglobulinemia, defects in phagocytosis or ciliary function, neutropenia, functional or anatomical asplenia, or a reduction in CD4_ T lymphocyte counts are all host defense deficits that can result in increased frequency or severity of pneumonia. Viral infection of alveolar macrophages may explain in part the very high rate of pneumococcal disease in the HIVinfected population. Anatomical defects such as obstructed bronchus, bronchiectasis, or sequestration of a pulmonary segment all lead to recurrent pneumonia or the failure of pneumonia to resolve.
Pathology: The pathology of pneumonia manifests as four general patterns: lobar
pneumonia, bronchopneumonia, interstitial pneumonia, and miliary pneumonia. Lobar
Pneumonia Lobar pneumonia classically involves an entire lung lobe relatively homogeneously.
There are four stages of lobar pneumonia. The first stage—congestion—occurs during the first 24 h and is characterized grossly by redness and a doughy consistency and microscopically by vascular congestion and alveolar edema. At this stage, many bacteria are present and are swept by the rapid expansion of edema fluid throughout the lobe via the pores of Kohn. Only a few neutrophils are seen at this stage. The second stage—termed red hepatization because of the color of the lung and the similarity of its airless, noncrepitant firmness to the consistency of liver —is characterized microscopically by the presence of many erythrocytes, neutrophils, desquamated epithelial cells, and fibrin in the alveolar spaces. In the third stage—gray hepatization—the lung is dry, friable, and gray-brown to yellow as a consequence of a persistent fibrinopurulent exudate, a progressive disintegration of red blood cells, and the variable presence of hemosiderin. The exudate contains macrophages as well as neutrophils, but bacteria are seldom visible. The second and third stages last for 2 to 3 days each, with a 2- to 6-day duration of maximal consolidation. The final stage—resolution—is characterized by enzymatic digestion of the alveolar exudate; resorption, phagocytosis, or coughing up of the residual debris; and restoration of the pulmonary architecture. Bronchopneumonia Bronchopneumonia, a patchy
consolidation involving one or several lobes. The neutrophilic exudate is centered in bronchi and bronchioles, with centrifugal spread to the adjacent alveoli and diminishing cellular exudate; often there is only edema in the periphery of the lesion. Interstitial Pneumonia Interstitial
pneumonia is defined by histopathologic identification of an inflammatory process predominantly involving the interstitium, including the alveolar walls and the connective tissue around the bronchovascular tree. The alveolar septa contain an infiltration of lymphocytes, macrophages, and plasma cells. The alveoli do not contain a significant exudate, but protein-rich hyaline membranes may line the alveolar spaces. Miliary Pneumonia The original description
of miliary pneumonia was based on the resemblance of the diffusely distributed 2- to 3-mm lesions of hematogenous tuberculosis to millet seeds. The current concept of miliary pneumonia is based on its numerous discrete lesions resulting from the spread of the pathogen to the lungs Classification
Clinical Manifestations: Pneumonia can range in severity from mild to fulminant and
fatal, with serious disease developing even in previously healthy persons. The onset may be sudden and dramatic or insidious. Fever, cough (nonproductive or productive of purulent or rust- colored sputum), pleuritic chest pain, chills or rigors, and shortness of breath are typical—albeit nonspecific—manifestations of pneumonia. Symptoms reported with some frequency include headache, nausea, vomiting, diarrhea, myalgia, arthralgia, and/or fatigue. Falls and new-onset or worsening confusion may be important manifestations in an elderly person. The physical signs associated with pneumonia are tachypnea, dullness to percussion, increased tactile and vocal fremitus, egophony, whispering pectoriloquy, crackles, and pleural friction rub. A diagnosis of pneumonia should be confirmed by chest radiography. Lab Studies: Leukocytosis with a left shift, although commonly observed in any bacterial
infection, may be absent in patients who are elderly or debilitated. Leukopenia (defined as a WBC count of <5000) is an ominous sign of impending sepsis and portends a poor outcome. Tests for ethiologic may include the following: blood culture, sputium stains and
culture detection, serology, polymerase chain reaction, detection of antigens of pulmonary Imaging Studies: Chest radiograph findings may indicate the following: a segmental or
lobar opacity with air bronchogram, cavitary lesions and bulging lung fissures, presence of cavitation and associated pleural effusions, tendency to involve the upper lung zones Other Tests
Arterial blood gas (ABG) determination: Evaluation of the patient's gas exchange is essential in order to decide if hospital admission, oxygen supplementation, or other efforts are Pulse oximetry of less than 90% indicates significant hypoxia; an ABG determination Bronchoscopy: Bronchial washing specimens can be obtained. Protected brush and bronchoalveolar lavage can be performed for quantitative cultures. Transtracheal aspiration for culture: This procedure is mentioned primarily for historical significance. This method of obtaining lower respiratory secretions has been replaced by Thoracentesis: This is an essential procedure in patients with a parapneumonic pleural effusion. Obtaining fluid from the pleural space for laboratory analysis allows for the differentiation between simple and complicated effusions. This determination helps guide further Diagnosis: The usual standard for the diagnosis of pneumonia is chest radiography,
which, however, is not 100% sensitive. High-resolution computed tomography (CT)occasionally detects pulmonary opacities in patients with symptoms and signs suggestive of pneumonia in whom chest radiographs are reported as not showing pneumonia. Differential diagnosis: Atelectasis, Bronchiectasis, Chronic Bronchitis, Chronic
Obstructive Pulmonary Disease, Foreign Body Aspiration, Influenza, Klebsiella Infections, Lung ycobacterium Avium-Intracellulare , Mycobacterium Kansasii, Pneumococcal Infections, Psittacosis, Respiratory Failure, Bacterial Sepsis.
1. Assess pneumonia severity. Pay attention to vital signs, including oxygen saturation. Always count the respiratory rate yourself for 1 min.
2. Ensure adequate oxygenation and support of circulation.
3. Perform etiologic workup (dictated by pneumonia severity).
4. Determine site of treatment: home, hospital (ward or intensive care 5. Institute empirical antibiotic therapy.
6. Rule out empyema in all patients with a pleural effusion of _1 cm on lateral decubitus chest 7. Never forget tuberculosis and Pneumocystis infection as possible etiologies. Check your hospital policy regarding the isolation of patients. In some centers where tuberculosis is common, all patients are isolated until sputum smears are found to be negative for acid-fast 8. Consider pulmonary embolus in all patients with pleuritic chest pain.
9. Consider end-of-life decision-making.
10. Monitor and treat comorbid illnesses.
11. Monitor for achievement of stability of selected physiologic parameters.
12. Assess ability to perform activities of daily living.
14. Consider preventive measures: a. Smoking cessation counseling (if appropriate) b. Assessment of pneumococcal and influenza vaccination status, with vaccine administration as necessary c. Assessment of risk of aspiration and institution of preventive measures 15. Follow up to ensure radiographic clearance of pneumonia. All patients >40 years old and all tobacco smokers should have a follow-up chest radiograph to document pneumonia resolution.
Initial Empirical Antibiotic Therapy for Community-Acquired Pneumonia Treatment Setting; Patient’s Condition Regimena Outpatient; no cardiopulmonary disease, no risk factors for DRSP infection: Macrolide (e.g., clarithromycin 500 mg bid PO x 10 days; or azithromycin 500 mg PO once, then 250 mg/d x 4 days) or Doxycycline 100 mg bid PO _ 10 days Outpatient; cardiopulmonary disease and/or (1) risk factors for DRSP infection or (2)high DRSP prevalence in community: Quinolone with enhanced activity against Streptococcus pneumoniae—e.g., levofloxacin 500 mg/d PO (or, with Ccr <50 mL/min, 250 mg/d), moxifloxacin 400 mg/d PO, or gatifloxacin 400 mg/d PO or _-Lactam (cefpodoxime 200 mg bid, cefuroxime axetil 750 mg tid, or amoxicillin 1000 mg tid, PO; amoxicillin/clavulanic acid 875/175 mg tid)plus macrolide or doxycycline or Telithromycin 800 mg q24h _ 10 days Hospital ward Cefuroxime 750 mg q8h IV or ceftriaxone 1 g/d IV or cefotaxime 2 g q6h IV or ampicillin/ sulbactam 1.5–3 g q6h IV plus Azithromycin 1 g/d IV followed by 500 mg/d IV or Quinolone with enhanced activity against S. pneumoniae (see above) Intensive care unit; no risk factors for Pseudomonas aeruginosa infection Azithromycin 1 g IV, then start 500 mg IV 24 h later plus Ceftriaxone 1 g q12h IV or Cefotaxime 2 g q6h IV or Intensive care unit; risk factors for P. aeruginosab Imipenem (or meropenem)500 mg q6h IV or Piperacillin/tazobactam 3.375 g q6h IV plus Ciprofloxacin 750 mg q8h IV Nursing home Amoxicillin/clavulanic acid 875/125 mg tid PO plus Macrolide PO (see above) or Quinolone PO with enhanced activity against S. pneumoniae (see above) or Ceftriaxone 500–1000 mg/d IM or cefotaxime 500 mg IM q12h plus Macrolide (see above) Aspiration pneumonitis (presumed to be due to effects of gastric acid or other irritants) Wait 24 h; if symptoms persist, give antibiotic therapy delineated below for aspiration Aspiration pneumonia; poor dental hygiene or putrid sputum, alcoholism (anaerobic infection suspected) Metronidazole 500 mg q12h POe or Piperacillin/tazobactam 3.375 g q6h IV or Imipenem 500 mg q6h IV plus One of the following: levofloxacin 500 mg/d IV or PO, moxifloxacin 400 mg/d PO, gatifloxacin 400 mg/d IV or PO, ceftriaxone, or cefotaxime Aspiration pneumonia; community-acquired Levofloxacin, moxifloxacin, gatifloxacin, Concomitant meningitis (suspected pneumococcal) Vancomycin 1 g q12h IV plus Criteria for Hospital Admissionof an Adult with Community-Acquired Pneumoniaa
2. Systolic blood pressure _90 mmHg or 30 mmHg below baseline 3. New-onset confusion or impaired level of consciousness 4. Hypoxemia: PO _60 mmHg while breathing room air or oxygen 2 saturation _90% 5. Unstable comorbid illness (e.g., decompensated congestive heart failure, uncontrolled diabetes mellitus, alcoholism, immunosuppression) 6. Multilobar pneumonia, if hypoxemia is present 7. Pleural effusion that is _1 cm on lateral decubitus chest radiography and has the characteristics of a complicated parapneumonic effusion on pleural fluid analysis Other inpatient care
Adequate respiratory support (eg, low-flow oxygen, assisted ventilation) is provided as dictated by the patient's clinical situation. Bronchial hygiene includes suctioning of secretions, chest physiotherapy, and positioning to encourage dependent drainage. These are used to optimize the elimination of purulent sputum General supportive measures include proper hydration, nutrition, and patient ambulation.
Prognosis: Pneumonia is the sixth leading cause of death in the United States and is the
most common infectious cause of death. The mortality rate is reported to be 1% in the outpatient setting but may increase to up to 25% in those requiring hospital admission. In a patient with preexisting respiratory disease, onset of bacterial pneumonia may result in deterioration of respiratory status, leading to respiratory failure and death. Nosocomial pneumonia is the leading cause of death among hospital-acquired infections. Recent studies have shown that nosocomial pneumonia causes excessive risk of death, and the mortality rates range from 20-50%. BRONCHIECTASIS
DEFINITION 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. Although this definition is based on pathologic changes in the bronchi, diagnosis is often suggested by the clinical consequences of chronic or recurrent infection in the dilated airways and the associated secretions that pool within Epidemiology. Bronchiectasis is relatively uncommon with a prevalence of around 100,000
cases. Bronchiectasis is a major cause of morbidity in less-developed countries, especially in countries with limited access to medical care and antibiotic therapy.
ETIOLOGY Infectious Causes Virulent bacterial infections, especially with potentially
necrotizing organisms such as Staphylococcus aureus, Klebsiella, and anaerobes, remain important causes of bronchiectasis when antibiotic treatment of a pneumonia is not given or is Noninfectious Causes Some cases of bronchiectasis are associated with 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, though the latter problem is often also complicated by aspiration of bacteria. Bronchiectasis also occurs rarely in ulcerative colitis, PATHOGENESIS Bronchiectasis is a consequence of inflammation and destruction of the
structural components of the bronchial wall. Infection is the usual cause of the inflammation; microorganisms such as Pseudomonas aeruginosa and Haemophilus influenzae produce pigments, proteases, and other toxins that injure the respiratory epithelium and impair mucociliary clearance. The host inflammatory response induces epithelial injury, largely as a result of mediators released from neutrophils. As protection against infection is compromised, the dilated airways become more susceptible to colonization and growth of bacteria. Thus, a reinforcing cycle can result, with in- flammation producing airway damage, impaired clearance of microorganisms, and further infection, which then completes the cycle by inciting more PATHOLOGY 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, including cartilage, muscle, and elastic tissue, are destroyed and may be replaced by fibrous tissue. Three different patterns of bronchiectasis were described: cylindrical bronchiectasis, varicose bronchiectasis. saccular (cystic) bronchiectasis. CLINICAL MANIFESTATIONS Patients typically present with persistent or recurrent cough
and purulent sputum production. Hemoptysis occurs in 50 to 70% of cases and can be due to bleeding from friable, inflamed airway mucosa. More significant, even massive bleeding is often a consequence of bleeding from hypertrophied bronchial arteries. When a specific infectious episode initiates bronchiectasis, patients may describe a severe pneumonia followed by chronic cough and sputum production. Alternatively, patients without a dramatic initiating event often describe the insidious onset of symptoms. In some cases, patients are either asymptomatic or have a nonproductive cough, often associated with “dry” bronchiectasis in an upper lobe.
Dyspnea or wheezing generally reflects either widespread bronchiectasis or underlying chronic obstructive pulmonary disease. With exacerbations of infection, the amount of sputum increases, it becomes more purulent and often more bloody, and patients may become febrile. Such episodes may be due solely to exacerbations of the airway infection, but associated parenchymal infiltrates sometimes reflect an adjacent pneumonia. Physical examination of the chest overlying an area of bronchiectasis is quite variable. Any combination of crackles, rhonchi, and wheezes may be heard, all of which reflect the damaged airways containing significant secretions. As with other types of chronic intrathoracic infection, clubbing may be present. Patients with severe, diffuse disease, particularly those with chronic hypoxemia, may have associated cor pulmonale and right ventricular failure. Amyloidosis can result from chronic infection and inflammation but Lab Studies: 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. Additional evaluation is aimed at diagnosing the RADIOGRAPHY Though the chest radiograph is important in the evaluation of suspected
bronchiectasis, the findings are often nonspecific. At one extreme, the radiograph may be normal Bronchography, which involves coating the airways with a radiopaque, iodinated lipid dye instilled through a catheter or bronchoscope, can provide excellent visualization of bronchiectatic airways. However, this technique has now been replaced by computed tomography (CT), which also provides an excellent view of dilated airways as seen in cross- sectional images (Fig. 240-1). With the advent of high-resolution CT scanning, in which the images are 1.0 to 1.5 mm thick, the sensitivity for detecting bronchiectasis has improved even Diagnosis Imaging studies, especially high-resolution CT (HRCT) scanning, are the
cornerstone for the diagnosis of bronchiectasis.
Differential diagnosis: Alpha1-Antitrypsin Deficiency, A
TREATMENT Therapy has four major goals: (1) elimination of an identifiable
underlying problem; (2) improved clearance of tracheobronchial secretions; (3) control of infection, particularly during acute exacerbations; and (4) reversal of airflow obstruction.
Appropriate treatment should be instituted when a treatable cause is found, for example, treatment of hypogammaglobulinemia with immunoglobulin replacement, tuberculosis with antituberculous agents, and ABPA with glucocorticoids. Secretions are typically copious and thickand contribute to the symptoms. A variety of mechanical methods and devices accompanied by appropriate positioning can facilitate drainage in patients with copious secretions. Mucolytic agents to thin secretions and allow better clearance are controversial. Aerosolized recombinant DNase, which decreases viscosity of sputum by breaking down DNA released from neutrophils, has been shown to improve pulmonary function in cystic fibrosis, but similar benefits have not been found with bronchiectasis due to other etiologies. Antibiotics have an important role in management. For patients with infrequent exacerbations characterized by an increase in quantity and purulence of the sputum, antibiotics are commonly used only during acute episodes.
Although choice of an antibiotic may be guided by Gram’s stain and culture of sputum, empiric coverage (e.g., with ampicillin, amoxicillin, trimethoprim-sulfamethoxazole, or cefaclor) is often given initially. When P. aeruginosa is present, oral therapy with a quinolone or parenteral therapy with an aminoglycoside or thirdgeneration cephalosporin may be appropriate. In patients with chronic purulent sputum despite short courses of antibiotics, more prolonged courses, e.g., with an oral antibiotic or inhaled aminoglycosides, or intermittent but regular courses of single or rotating antibiotics have been used. Bronchodilators to improve obstruction and aid clearance of secretions are particularly useful in patients with airway hyperreactivity and reversible airflow obstruction. Although surgical therapy was common in the past, more effective antibiotic and supportive therapy has largely replaced surgery. However, when bronchiectasis is localized and the morbidity is substantial despite adequate medical therapy, surgical resection of the involved region of lung should be considered. When massive hemoptysis, often originating from the hypertrophied bronchial circulation, does not resolve with conservative therapy, including rest and antibiotics, therapeutic options are either surgical resection or bronchial arterial embolization. Although resection may be successful if disease is localized, embolization is preferable with widespread disease. In patients with extensive disease, chronic hypoxemia and cor pulmonale may indicate the need for long-term supplemental oxygen. For selected patients who are disabled despite maximal therapy, lung transplantation is a therapeutic option.
Prognosis: 10-year mortality rates is 28%. Currently, mortality is more often related to
progressive respiratory failure and cor pulmonale than to uncontrolled infection. Life-threatening hemoptysis may also occur but is uncommon.
A pleural effusion is fluid in the pleural space. Effusions can be divided by their protein concentration into transudates (<25g/L) and exudates (>35g/L), see OPPOSITE. Blood in the pleural space is a haemothorax; pus in the pleural space is an empyema, and chyle (lymph with fat) is a chylothorax. Both blood and air in the pleural space is called a haemopneumothorax.
Transudates may be due to ↑ venous pressure (cardiac failure, constrictive pericarditis, fluid overload), or hypoproteinaemia (cirrhosis, nephrotic syndrome, malabsorption). Also occur in hypothyroidism and Meigs' syndrome (right pleural effusion and ovarian fibroma). Exudates are mostly due to increased leakiness of pleural capillaries secondary to infection, inflammation, or malignancy. Causes: pneumonia; TB; pulmonary infarction; rheumatoid arthritis; SLE; bronchogenic carcinoma; malignant metastases; lymphoma; mesothelioma; lymphangitis Symptoms
Asymptomatic or dyspnoea, pleuritic chest pain.
Decreased expansion; stony dull percussion note; diminished breath sounds occur on the affected side. Tactile vocal fremitus and vocal resonance are ↓ (inconstant and unreliable).
Above the effusion, where lung is compressed, there may be bronchial breathing and aegophony (bleating vocal resonance). With large effusions there may be tracheal deviation away from the effusion. Look for aspiration marks and signs of associated disease: malignancy (cachexia, clubbing, lymphadenopathy, radiation marks, mastectomy scar); stigmata of chronic liver disease; cardiac failure; hypothyroidism; rheumatoid arthritis; butterfly rash of SLE.
Small effusions blunt the costophrenic angles, larger ones are seen as water-dense shadows with concave upper borders. A completely horizontal upper border implies that there is is useful in identifying the presence of pleural fluid and in guiding diagnostic or Percuss the upper border of the pleural effusion and choose a site 1 or 2 intercostal spaces below it. Infiltrate down to the pleura with 5–10mL of 1% lidocaine. Attach a 21G needle to a syringe and insert it just above the upper border of an appropriate rib (avoids neurovascular bundle). Draw off 10–30mL of pleural fluid and send it to the lab for clinical chemistry (protein, glucose, pH, LDH, amylase); bacteriology (microscopy and culture, auramine stain, TB culture); cytology and, if indicated, immunology (rheumatoid factor, ANA, complement).
If pleural fluid analysis is inconclusive, consider parietal pleural biopsy with an Abrams' needle. Thoracoscopic or CT-guided pleural biopsy increases diagnostic yield (by enabling direct visualization of the pleural cavity and biopsy of suspicious areas).
Drainage If the effusion is symptomatic, drain it, repeatedly if necessary. Fluid is best removed slowly (≤2L/24h). It may be aspirated in the same way as a diagnostic tap, or using an intercostal drain (see p750).
Pleurodesis with tetracycline, bleomycin, or talc may be helpful for recurrent effusions.
Thorascopic talc pleurodesis is most effective for malignant effusions. Empyemas (p176) are best drained using a chest drain, inserted under ultrasound or CT guidance.
Intrapleural streptokinase Probably no benefit.
Surgery: Persistent collections and increasing pleural thickness (on ultrasound) requires


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