Inflammatory and suppurative diseases of lungs
Inflammatory and suppurative diseases of lungs
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
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
, Moraxella catarrhalis
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.
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.
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
—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
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
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.
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
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
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
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.
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:
(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
—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
Quinolone with enhanced activity against S. pneumoniae
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
Piperacillin/tazobactam 3.375 g q6h IV plus
Ciprofloxacin 750 mg q8h IV
Amoxicillin/clavulanic acid 875/125 mg tid PO plus
Macrolide PO (see
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
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.
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.
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 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
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
, and anaerobes, remain
important causes of bronchiectasis when antibiotic treatment of a pneumonia is not given or is
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,
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
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
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
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
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
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
Imaging studies, especially high-resolution CT (HRCT) scanning, are the
cornerstone for the diagnosis of bronchiectasis.
Alpha1-Antitrypsin Deficiency, A
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.
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 â†‘ 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
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 â†“ (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 5â€“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 10â€“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 (â‰¤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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