Respiratory mechanics and sounds: ( Fig. 28.1 )
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Inspiration:
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Active process in which diaphragmatic contraction generates negative intrathoracic pressure, sucking air into the conducting airways
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Exhalation:
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Passive process in which intrinsic chest wall and lung compliance generate positive intrathoracic pressure, forcing air out of the thorax
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Extrathoracic stridor:
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High-pitched, monophonic, isolated inspiratory sound implying extrathoracic, upper airway/laryngeal obstruction, as occurs from mucus, swollen tissue, external compression, or tumor
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Upper airway and laryngeal structures outside of the chest collapse during inspiration and open during expiration
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Stridor requires urgent evaluation because upper airway obstruction may necessitate an emergency surgical airway
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Wheeze:
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Harmonic, polyphonic sound indicating intrathoracic airway obstruction
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Airway structures inside the chest collapse during expiration and open during inspiration
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Mild airway narrowing causes an isolated expiratory wheeze
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Severe airway narrowing causes an inspiratory and expiratory wheeze
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An isolated inspiratory wheeze equals extrathoracic stridor until proven otherwise (examine the neck)
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It is not possible for an airway structure inside the chest to produce an isolated inspiratory wheeze
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Smoking cessation
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Getting a smoker to quit smoking is one of the greatest interventions you can make as a physician
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You must approach smoking cessation with the certainty that every patient will quit
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Your patients must feel your commitment and certainty that they will quit
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Active smokers coming to a pulmonary clinic feel ashamed and want to quit, no matter what they say
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Active smokers with lung disease employ elaborate denial schemes, constantly looking for tacit approval and acceptance from the pulmonologist:
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“I’ll never quit … throw a pack in the grave with me” equals “it’s an impossible task doc”
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“It’s too late now … the damage is done” equals “it’s not worth it at this point”
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“I feel great and have no problem exercising” equals “there will be time to quit before trouble”
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“I’ve cut down to just three cigarettes a day” equals “good enough, eh doc?”
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“It’s the only joy I have in my life” equals “have pity on me doc (I am horribly depressed)”
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Tacit approval is given when:
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You forget to discuss smoking cessation; you might as well light up a cigarette for the patient
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Counseling works and does not have to take much time
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It should be the first and last thing you discuss with every active smoker, without alienating him or her
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You accept any of the patient’s rationalizations
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Each rationalization must be addressed and exposed for the excuse that it is
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“I’ll never quit” is parried with “everyone quits eventually and wishes they had done it earlier”
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“It’s too late now” is parried with “things can get much worse; imagine getting out of breath taking a shower”
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“I feel great” is parried with a cautionary tale (based on many true stories) about ventilatory limitation and how it can appear suddenly:
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“Doc, I was fine 2 weeks ago, got pneumonia, and now can’t walk up a flight of steps, and you’re telling me it’s emphysema?” Yes
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“I’ve cut down to just three cigarettes a day” is parried with “fabulous, but now the hard work begins”
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After you make it clear that you are serious about smoking cessation by not accepting the patients’ initial rationalizations, start by explaining your perspective:
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Smoking is destroying their lungs and is going to cause cancer, heart attack, or stroke
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Point out the irrationality of worrying about other disease prevention (ie, daily aspirin, screening colonoscopy) while they are smoking
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Smoking poses such a grave risk to health that it eclipses the benefits of any primary disease prevention measure
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Explain that this irrationality in their behavior occurs because it’s an addiction:
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Explain that there is a cluster of neurons in their brain always trying to convince them to smoke
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“It’s a great day … time to celebrate with a cigarette”
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“It’s a crappy day … I need a cigarette”
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“It’s such a boring day … nothing to do but smoke”
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Ask them if they have ever quit, how they quit, and what made them relapse
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It is an addiction (with all the shame, lack of self-control, etc), so be empathetic
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Remind them that the successful ex-smokers quit and relapse an average of 10 times before durable cessation
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Each failed attempt must be seen as the necessary work required by the difficult process of quitting
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Each quit-relapse attempt should be seen like a notch in their belt
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Active smokers in a pulmonary clinic must always be in the process of quitting
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Common second-line rationalizations:
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In response to nicotine supplements, “I’m just trading one addiction for another”
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Nicotine supplements are much safer than tobacco products and not nearly as addictive
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Almost nobody chews the gum forever
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“It’s not safe for me to smoke and use the supplements, and I might cheat”
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Smoking is not safe
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Educate patients on nicotine toxicity (potentially incapacitating vertigo, horizontal nystagmus, and nausea)
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Such that they should not “cheat” while driving or climbing a ladder
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Nicotine toxicity often produces a conditioned taste aversion to tobacco, which is useful in quitting
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Never let your inpatients go out and smoke:
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Offer them anything else for their craving while they are an inpatient (from nicotine to lorazepam)
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If you cannot help them quit in the new context of being an inpatient, you are not trying
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Nicotine patches in the intensive care unit increase cardiovascular events, such that they should not be used for intubated, sedated patients in attempts to reduce sedation needs
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Helping while they are quitting:
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Handling the proud report “I’ve cut down to just three cigarettes a day”:
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Smoking (and addiction in general) is context dependent
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The last three to five cigarettes a day are the “pillar” cigarettes
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Those that the smoker falsely believes, they will always long for
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Typically with their morning coffee, after dinner, during their commute to work, and while on their work break
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At this stage, cessation efforts must focus on breaking the habit
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Tell your smokers they can have their three cigarettes a day but not at the time they want
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They must wait at least 2 hours (encourage them to use nicotine supplements [eg, gum] during that time)
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Encourage them to change their behavior, to avoid contexts that provoke craving (eg, eat, drink, and take breaks in different locations with different, nonsmoking people)
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Calling a patient on their quit date is a spectacular way to show that you are invested in their quitting (put it on your calendar)
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Much easier for people to fail themselves than to fail people they respect
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Remind them that the chemical addiction to cigarettes lasts 2 weeks, and after that point, it is behavioral
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Creates a concrete, achievable goal that is easier to focus on than lifetime abstinence
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Bronchiectasis
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Bronchiectasis is:
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Not related to smoking or chronic obstructive pulmonary disease (COPD)
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The term used to describe an airway that fails to taper normally, making its lumen abnormally large for its airway generation
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The vessel traveling alongside the airway gives a good approximation of its anticipated size
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Caused by either:
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Fibrosis of the parenchyma surrounding the airway, dilating via traction (ie, traction bronchiectasis), as seen in pulmonary fibrosis, radiation fibrosis, and nontuberculous mycobacteria (NTM) infection
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Bronchiectasis occurs in the areas of fibrosis
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Mucus plugging with prolonged airway impaction, as seen in allergic bronchopulmonary aspergillosis (ABPA) or as a sequela of a poorly treated bacterial pneumonia
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Bronchiectasis occurs focally or multifocally
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Cystic fibrosis, immune deficiency (eg, IgG), and ciliary dyskinesia (eg, Kartagener syndrome)
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Bronchiectasis occurs diffusely
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The most common cause of massive hemoptysis:
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Areas of bronchiectatic lung are poorly drained, chronically infected, and subject to pathologic angiogenesis, leading to large ecstatic bronchial and intercostal arteries prone to rupture
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Both a clinical syndrome (chronic daily purulence with intermittent acute infection) and a radiographic finding (which may be insignificant and asymptomatic)
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Bronchiectasis causes disease by impairing the ability of cough to clear secretions (necessary to prevent lung infection)
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Cough works by collapsing all but the main airways, expelling intraluminal material mechanically and via high expiratory flow rates
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Bronchiectatic areas fail to collapse and expel material normally, such that secretions pool, promoting chronic airway infection
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Chronic airway infection leads to:
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Persistent daily purulence (experienced as a chronic productive cough)
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Acute exacerbations in which patients complain of increased sputum, fever, and hemoptysis
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Sputum cultures often reveal multiple organisms and/or aerobic gram negative rods
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Outpatient management of bronchiectasis:
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Reduction of chronic purulence and cough requires daily airway secretion clearance via:
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Position (ie, postural drainage), in which the patient positions himself or herself in such a way that bronchiectatic areas are nondependent, allowing secretions to drain via gravity to more proximal airways where they may be cleared by cough
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Vibratory kinetic energy, in which the airway is vibrated, dislodging secretions and moving them proximally where they can be cleared by cough
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Airway vibration may be generated by either:
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An expiratory flow device with an oscillating resister (eg, flutter valve), in which the patient’s slow exhalation generates a vibrating column of air
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An external thoracic vest or wrap that vibrates the thorax externally
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Patients should understand that airway clearance devices (working appropriately) do not immediately cause large amounts of phlegm to be expelled, but rather, when performed several times every day, lead to a reduction in chronic purulence over weeks to months (akin to tooth brushing)
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If this is not explained, individuals may try their flutter valve once, not experience a satisfying episode of phlegm expulsion, and never use it again
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Nebulized hypertonic saline may be used to further help with secretion clearance
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Inhaled antibiotics (eg, tobramycin) are often helpful when individuals suffer from persistent/recurrent infection with a resistant organism (eg, pseudomonas)
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They are typically prescribed on and off for 2–4-week periods (to decrease the chance of resistance)
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When individuals complain of doing poorly during the off intervals, another antibiotic may be used (eg, ceftazidime)
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Inhaled antibiotics may still have efficacy (and may be used) even if the organism has demonstrated in vitro resistance, because of the high concentrations achieved in the airway mucosa
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Inhaled antibiotics may cause severe bronchospasm (necessitating discontinuation)
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Patients with bronchiectasis invariably develop acute exacerbations with fever, change in sputum (color/volume), and hemoptysis
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Mild to moderate exacerbations with scant hemoptysis and/or blood-tinged sputum may be treated on an outpatient basis with oral antibiotics
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Sputum cultures should be obtained in case empiric therapy fails
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That said, clinical success often occurs despite the presence of resistant organisms cultured (such that antibiotics should not be routinely broadened based on sputum culture results in the face of clinical success)
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Occasionally the true (sensitive) pathogen is overgrown by the resistant pseudomonas in the culture dish
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Severe exacerbations and/or those with significant hemoptysis should be treated on an inpatient basis
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Cultures should be obtained
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Broad-spectrum antibiotics should be administered intravenously (IV), even though WBC count and temperature are often normal
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Chest imaging should be performed
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Individuals with significant hemoptysis should have a chest computed tomography (CT) scan (arterial phase contrast if renal function permits) to localize the bleeding area and plan possible embolization
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Bronchoscopy adds very little to localization and may precipitate respiratory failure (see CH 24 )
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Interventional radiology (IR) should be consulted
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~ 85% of inpatient exacerbations with hemoptysis respond well to antibiotics with improvement in sputum and hemoptysis over 24–48 hours
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At this point individuals may be discharged to complete a course of IV antibiotics at home (via peripherally inserted central catheter line) or oral antibiotics if resistance patterns allow
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~ 15% of inpatient exacerbations are complicated by massive hemoptysis requiring embolization by interventional radiology
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IR embolization comes with the risk of spinal cord infarction (see CH 24 )
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Atypical and typical pneumonia (definitions and things to consider)
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Atypical and typical pneumonia are terms that carry different meanings in different contexts
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Clinically:
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Typical pneumonia presentation implies acute onset fever, productive cough, and a new infiltrate
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Atypical pneumonia presentation implies a more indolent course over weeks to months, involving low-grade temperatures/night sweats, dry cough, and infiltrate(s)
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Radiographically:
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Typical pneumonia appears as a lobar consolidation or as areas of dense consolidation (with clear air bronchograms)
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Atypical pneumonia may have many different radiographic appearances, including diffuse or focal ground glass, increased interstitial markings, nodules, and tree and bud opacities
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Organisms and route of infection:
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Typical pneumonia organisms (eg, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus ) cause the majority of community-acquired pneumonias
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They tend to have a typical pneumonia presentation and imaging
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These organisms are present in the naso/oral pharynx in 25% of the population at any time
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Infection occurs when an individual is carrying an organism in his or her naso/oral pharynx and he or she experiences a microaspiration event in the setting of impaired host immunity (eg, the postviral state)
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Atypical pneumonia organisms exist in a wider range of species (bacteria and fungi):
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Mycoplasma and chlamydia tend to cause an atypical clinical syndrome with atypical diffuse imaging
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Infection occurs person to person (likely by droplet)
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Most infections are very mild, despite radiographic infiltrates (a.k.a. walking pneumonia)
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Hypoxemia is unusual
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Self-resolving
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Legionella causes a typical pneumonia presentation with typical imaging (often with rounded, dense consolidations involving the right-middle and right-lower lobes)
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Initial deterioration after presentation is common, as well as associated gastrointestinal complaints
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Legionella is contracted by inhalation of contaminated water vapor
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NTM infection may be clinically silent or have atypical pneumonia characteristics
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Radiographically, NTM causes areas of dense consolidation with traction bronchiectasis and tree and bud nodules (± mediastinal adenopathy)
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NTM infection occurs with inhalation of contaminated water (often during showering)
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NTM organisms are found in tap water because they are not killed by chlorine
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Most NTM infections are low grade (involving asymptomatic fleeting nodules) and do not require treatment
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Indications for treatment include systemic symptoms (weight loss, fevers), progressive parenchymal destruction (increasing areas of traction bronchiectasis), and worsening restriction on pulmonary function tests
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Tuberculous mycobacterial (TB) infection
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Primary TB has a muted atypical pneumonia presentation with weeks of coughing and typical pneumonia imaging (often with necrosis)
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Reactivation TB also has an atypical presentation with months of coughing and systemic symptoms (weight loss/night sweats) and imaging showing upper lobe nodular/fibrocavitary infiltrates
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Aspergillus (see CH 10 )
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Endemic fungus (inhaled from the environment)
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Cryptococcus (in the immunocompetent) causes a typical pneumonia presentation with cough, chest pain fever, hemoptysis
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Imaging shows consolidations that may be mass-like (round and solid)
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Coccidiomycosis may cause both typical and atypical presentations depending on the individual’s ability to handle the organism
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Radiographically, cocci may cause lobar consolidation, mass-like consolidation, hilar and mediastinal adenopathy, or a cavitary lesion (ultimately persisting as a thin-walled cavity)
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Oral anaerobes (see CH 11 )
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