Tutorial 2: Pneumonia Flashcards

1
Q

What is CAP?

A

community-acquired pneumonia: acute infection of the pulmonary parenchyma acquired outside of the hospital

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2
Q

What are the two categories of nosocomial pneumonia?

A

hospital-acquired pneumonia (HAP)

ventilator-associated pneumonia (VAP)

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3
Q

What is HAP?

A

hospital-acquired pneumonia: pneumonia acquired ≥48 hours after hospital admission, and did not appear to be incubating at the time of admission.

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4
Q

What is VAP?

A

ventilator-associated pneumonia: pneumonia acquired ≥48 hours after endotracheal intubation.

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5
Q

What was HCAP, and how is it treated now?

A

Health care-associated pneumonia; currently treated as CAP

Referred to pneumonia acquired in health care facilities (eg, nursing homes, hemodialysis centers) or after recent hospitalization

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6
Q

What are the non-modifiable (/less modifiable) risk factors for pneumonia?

A
  • Older age (≥65)
  • Chronic comorbidities
  • Viral respiratory tract infection
  • Impaired airway protection (LOC, dysphagia)
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7
Q

What chronic comorbidities are risk factors for CAP?

A

COPD (comorbidity with highest risk for hospitalization)

  • other chronic lung disease (bronchiectasis, asthma)
  • CHF and other chronic heart disease
  • stroke
  • DM
  • malnutrition
  • immunocompromise
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8
Q

Once you have one risk factor for CAP, does having more increase your risk?

A

Yes: risk factors are additive

eg CHF, smoking, COPD

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9
Q

What are the three categories of most common causes of CAP?

A

Typical bacteria
Atypical bacteria
Respiratory viruses

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10
Q

What is the single most common bacterial cause of pneumonia?

A

Streptococcus pneumoniae (pneumococcus)

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11
Q

What pathogens are “typical bacterial” causes of CAP? (7 listed)

A
  • S. pneumoniae (most common bacterial cause)
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Staphylococcus aureus
  • Group A streptococci
  • Aerobic gram-negative bacteria (eg, Enterobacteriaceae such as Klebsiella spp or Escherichia coli)
  • Microaerophilic bacteria and anaerobes (associated with aspiration)
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12
Q

What pathogens are “atypical bacterial” causes of CAP? (5 listed)

A
  • Legionella spp
  • Mycoplasma pneumoniae
  • Chlamydia pneumoniae
  • Chlamydia psittaci
  • Coxiella burnetii
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13
Q

What defines “atypical” bacterial causes of CAP?

A
  • resistant to beta-lactams

- can’t be visualized on Gram stain or cultured using traditional techniques

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14
Q

What respiratory viruses cause CAP? (8 listed)

A
  • Influenza A and B viruses
  • Rhinoviruses
  • Parainfluenza viruses
  • Adenoviruses
  • Respiratory syncytial virus
  • Human metapneumovirus
  • Coronaviruses (eg, Middle East respiratory syndrome coronavirus)
  • Human bocaviruses
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15
Q

What features are associated with CAP due to community acquired MRSA?

A
Necrotizing or cavitary pneumonia
Empyema
Gross hemoptysis
Septic shock
Respiratory failure
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16
Q

What recent discovery has changed our understanding of pneumonia?

A

Lung microbiome: lung parenchyma was previously thought to be sterile

e.g. change from pathogen colonization of sterile lung to pathogen competition with microbiome – and dysbiosis as a risk factor for pneumonia

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17
Q

What are the most common symptoms associated with CAP?

A
  • Cough (with or without sputum production)
  • dyspnea
  • pleuritic chest pain
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18
Q

What are the most common physical exam findings associated with CAP?

A
  • tachypnea (RR > 24: 45-70%; most sensitive sign in older pt)
  • increased WOB
  • adventitious breath sounds, including rales/crackles (about 1/3 of pt) and rhonchi
  • fever (80%, though freq absent in older pt)

Tactile fremitus, egophony, and dullness to percussion also suggest pneumonia.

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19
Q

What is the gold standard for diagnosis of pneumonia?

A

Infiltrate on CXR, in context of supportive clinical syndrome (eg, fever, dyspnea, cough, and sputum production)

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20
Q

What are the most common lab findings associated with CAP?

A
  • CBC: Leukocytosis (15-30), leftward shift
  • leukopenia can occur; generally poor prognosis
  • inflammatory markers (CRP< ESR, procalcitonin)
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21
Q

What other features might CAP present with (not most common, but not rare)?

A
  • GI (N/V/D)

- MS changes

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22
Q

What features on CXR are consistent with CAP?

A
  • lobar consolidations
  • interstitial infiltrates
  • cavitations
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23
Q

What if the CXR is negative, but you still really suspect pneumonia based on clinical picture?

A

CT

Esp if immunocompromised (less infl response so less infiltrate) or known exposure to pathogen that causes pneumonia (eg legionella)

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24
Q

Name 2 score tools used to calculate mortality and determine site of treatment for CAP

A

PSI (Pneumonia Severity Index), aka PORT score

CURB-65

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25
Q

When do you treat a pt with CAP as ambulatory?

A

Otherwise healthy
Normal vital signs aside from fever
No concern for complication

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26
Q

When do you admit a pt with CAP?

A

SpO2 <92% on RA (sig change from baseline)

Also consider for practical concerns like inability to take oral meds, functional impairment, social issues affecting adherence or followup

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27
Q

What groups are not well represented in CAP scoring, and should be considered for admission even with mild scores?

A

patients with early signs of sepsis, rapidly progressive illness, or suspected infections with aggressive pathogens

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28
Q

When do you admit a pt to ICU for CAP?

A
  • respiratory failure requiring mechanical ventilation

- sepsis requiring vasopressor support

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29
Q

What criteria support early ICU admission, due to anticipated progression to sepsis? (name 5; 9 listed)

A

Three of:

  • AMS
  • Hypotension requiring fluids
  • T < 36
  • RR ≥ 30
  • PaO2/FiO2 ratio ≤250
  • BUN ≥ 7 mmol/L
  • Leukocyte count <4
  • Platelet count <100
  • Multilobar infiltrates
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30
Q

What microbiologic testing of CAP should be performed in outpatients?

A

Outpt: none – empiric Abx good

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31
Q

What microbiologic testing of CAP should be performed in inpatients?

A
  • Blood cultures
  • Sputum Gram stain and culture
  • other tests based on risk factors, epidemiology, exposures (eg immunocompromised? PCJ, fungal, parasites, CMV)

[suspect these may be US-specific:]

  • Urinary antigen testing for S. pneumoniae
  • Testing for Legionella spp (polymerase chain reaction [PCR] when available, urinary antigen test as an alternate)-
  • consider flu test
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32
Q

What else is on the DDx for CAP?

A

Present with pulmonary infiltrate and cough:

  • Congestive heart failure with pulmonary edema
  • Pulmonary embolism
  • Pulmonary hemorrhage
  • Atelectasis
  • Aspiration or chemical pneumonitis
  • Drug reactions
  • Lung cancer
  • Collagen vascular diseases
  • Vasculitis
  • Acute exacerbation of bronchiectasis
  • Interstitial lung diseases (eg, sarcoidosis, asbestosis, hypersensitivity pneumonitis, cryptogenic organizing pneumonia)
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33
Q

How long do pulmonary infiltrates due to pneumonia take to resolve?

A

Weeks: if resolving in days, consider alternate Dx

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34
Q

What are the features of the CURB-65 score?

A
  • Confusion
  • BUN > 7 mmol/L
  • RR ≥ 30
  • Systolic BP < 90 mmHg or Diastolic BP ≤ 60 mmHg
  • Age ≥ 65

1 point outpt, 2 inpt or close f/u, 3+ inpt

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35
Q

What do empiric treatment regimens for outpt CAP target?

A

S. pneumoniae

Atypical pathogens

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36
Q

When would you expand your empiric coverage for outpt CAP?

A
  • comorbidities
  • smoking
  • recent Abx
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37
Q

When would you expand your empiric coverage for outpt CAP even further?

A

Structural lung disease

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38
Q

What would expansion of empiric coverage for outpt CAP target?

A

beta-lactamase-producing H. influenzae, M. catarrhalis, and methicillin-susceptible S. aureus

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39
Q

What would further expansion of empiric coverage for outpt CAP target?

A

Enterobacteriaceae, such as E. coli and Klebsiella spp

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40
Q

What is the initial empiric Abx regimen for pt with outpt CAP who are <65 years, otherwise healthy, and have not recently used antibiotics?

A

amoxicillin 1g TID
+
macrolide (eg azithromycin) or doxycycline
(macrolide preferred)

Some recommend amoxicillin alone to start

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41
Q

What is the initial empiric Abx regimen for pt with outpt CAP with

  • comorbidities
  • smoking
  • recent Abx?
A

oral extended-release amoxicillin-clavulanate (2 g twice daily)
+
macrolide (eg azithromycin) or doxycycline
(macrolide preferred)

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42
Q

What is the alternative to amoxicillin-based regimens?

A
  • combination therapy with a cephalosporin plus a macrolide or doxycyclin
    or,
  • monotherapy with lefamulin.
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43
Q

How long should you treat pt with outpt CAP with Abx?

A

5d, up to 7d; should be improving, and be afebrile for at least 48h before stopping

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44
Q

What do empiric treatment regimens for CAP treated as an inpt target?

A
  • typical pathogens (eg, S. pneumoniae, H. influenzae, and M. catarrhalis)
  • atypical pathogens (eg, Legionella pneumophilia, M. pneumoniae, and C. pneumoniae)
  • S. aureus
  • gram-negative enteric bacilli (eg, Klebsiella pneumoniae)
45
Q

What are the key factors in selecting an initial Abx regimen for inpt with CAP?

A

Risk of Pseudomonas and/or methicillin-resistant S. aureus (MRSA)

46
Q

What is the initial empiric Abx regimen for pt with inpt CAP without suspicion for MRSA or Pseudomonas?

A

combination therapy:

beta-lactam + macrolide
or
beta-lactam + fluoroquinolone

47
Q

What is the initial empiric Abx regimen for pt with inpt CAP with

  • known colonization with pseudomonas
  • recent hospitalization with Abx use
  • other strong suspicion for pseudomonas?
A

antipseudomonal beta-lactam + antipseudomonal fluoroquinolone (eg, ciprofloxacin or levofloxacin).

48
Q

What are the antipseudomonal beta lactams? (5 listed)

A
piperacillin-tazobactam
cefepime
ceftazidime
meropenem
imipenem
49
Q

What are the antipseudomonal fluoroquinolones? (2 listed)

A

Ciprofloxacin

levofloxacin

50
Q

What is the initial empiric Abx regimen for pt with inpt CAP with

  • known colonization or prior infection with MRSA
  • other strong suspicion for MRSA?
A

Treatment for non-pseudo/non-MRSA, or treatment for suspect MRSA,
+
agent with anti-MRSA activity, such as vancomycin or linezolid
(Linezolid preferred for suspected community acquired MRSA)

51
Q

What are the risk factors for MRSA?

A

known MRSA colonization or prior MRSA infection

  • recent antibiotic use (esp IV w/in last 3mo)
  • recent influenza-like illness
  • the presence of empyema
  • necrotizing/cavitary pneumonia
  • immunosuppression
52
Q

What are the risk factors for community acquired MRSA?

A
  • history of MRSA skin lesions
  • participation in contact sports
  • injection drug use
  • crowded living conditions
  • men who have sex with men
53
Q

What are the risk factors for pseudomonas?

A
  • known colonization or prior infection with Pseudomonas spp
  • recent hospitalization or antibiotic use
  • underlying structural lung disease (eg, CF or advanced COPD [bronchiectasis])
  • immunosuppression.
54
Q

When should you give adjunctive glucocorticoids in CAP?

A

Evidence not clear: generally, don’t.

Consider in pt with CAP with exaggerated or dysregulated host inflammatory response (refractory septic shock–look up criteria if it gets to this point).

55
Q

What subjective features should you monitor in pt with CAP?

A
  • cough
  • sputum production
  • dyspnea
  • chest pain
56
Q

What objective features should you monitor in pt with CAP?

A
  • temp
  • HR
  • RR
  • oxygenation
  • WBC
57
Q

How soon after treatment initiation do pt with CAP demonstrate improvement?

A

Generally, patients demonstrate some clinical improvement within 48 to 72 hours

58
Q

When should you discharge a pt who was admitted with CAP?

A
  • clinically stable
  • can take oral medication
  • no other active medical problems
  • safe environment for continued care
59
Q

What should you consider when managing immunocompromised patients presenting with presumed CAP?

A
  • can have different kinds of infections (eg fungal, PCP)
  • multiple infections can co-occur
  • SSx can be subtle and nonspecific

Consider involving multidisciplinary team.

60
Q

Why consider involving multidisciplinary team when managing immunocompromised patients presenting with presumed CAP?

A
  • management is complex
  • drug interactions are common
  • adjustments in immunosuppressive regimens may be needed
  • empiric treatment options can be associated with significant toxicity
61
Q

Should followup CXR be obtained to ensure pneumonia is resolved?

A

Most pt don’t need it if Sx are resolving within 5-7d.

Radiographic response lags behind clinical response.

62
Q

What are the two general categories of the ways patients with CAP fail clinically?

A
  • progression of initial infection

- development of comorbid complications (eg HAP, C diff, CV events)

63
Q

If pt don’t resolve within 5-7d with empiric ABx, they have non-resolving CAP. What are the main subcategories of non-resolving CAP?

A
  • delayed clinical response
  • loculated infection (abscess, empyema, other)
  • bronchial obstruction
  • Pathogens that cause subacute/chronic CAP (eg TB)
  • Incorrect initial Dx
64
Q

What is the mortality for CAP?

A

Range. 30 day mortality for…

  • Ambulatory: <1%
  • Severe: 20-25%
65
Q

What are the key strategies to prevent CAP? (3 listed)

A

Smoking cessation (when appropriate)

Influenza vaccination for all patients

Pneumococcal vaccination for at-risk patients

66
Q

What are most CAP caused by?

A

Streptococcus pneumoniae and respiratory viruses

67
Q

What are the categories of antimicrobial-resistant gram-negative bacilli according to the US and European CDCs?

A
Multidrug resistant (MDR) Extensively drug resistant (XDR)
Pandrug resistant (PDR)
68
Q

What is the definition of Multidrug resistant?

A

acquired nonsusceptibility to at least one agent in three different antimicrobial classes.

69
Q

What is the definition of extensively drug resistant?

A

nonsusceptibility to at least one agent in all but two antimicrobial classes.

70
Q

What is the definition of pandrug resistant?

A

nonsusceptibility to all antimicrobial agents that can be used for treatment.

71
Q

What proportion of healthy adults aspirate during sleep?

A

Approx 45%

72
Q

What is the primary route of lung infection?

A

microaspiration of organisms that have colonized the oropharyngeal tract (or, to a lesser extent, the gastrointestinal tract)

73
Q

What are common pathogens for HAP and VAP?

A

aerobic gram-negative bacilli (eg, Escherichia coli, Klebsiella pneumoniae, Enterobacter spp, Pseudomonas aeruginosa, Acinetobacter spp)

gram-positive cocci (eg, Staphylococcus aureus, including methicillin-resistant S. aureus [MRSA], Streptococcus spp)

Viruses, fungi becoming increasingly recognized

74
Q

How is HAP diagnosed?

A

clinical diagnosis:

new lung infiltrate
+
clinical evidence that the infiltrate is of infectious origin: new fever, purulent sputum, leukocytosis, decline in oxygenation

75
Q

What ventilator-specific findings might be present in someone with VAP?

A

Ventilator mechanics: reduced tidal volume, increased inspiratory pressures

76
Q

Name 3 common radiographic abnormalities in VAP

A

alveolar infiltrates, air bronchograms, and silhouetting of adjacent solid organs

77
Q

What diagnostic test should be performed in patients with suspected VAP?

A

Respiratory tract sample for microscopy and culture

Experts differ re invasive (eg bronchoalveolar lavage) vs noninvasive (eg aspiration) and quantitative vs non-quantitative

78
Q

What does microscopic analysis of respiratory tract samples tell you in VAP?

A

semi-quantitative analysis of polymorphonuclear leukocytes and other cell types, as well as the Gram stain.

Can be helpful in determining a possible pathogen and alter antibiotic selection

79
Q

How is VAP diagnosed?

A

new lung infiltrate
+
clinical evidence that the infiltrate is of infectious origin: new fever, purulent sputum, leukocytosis, decline in oxygenation
+
resp sample positive (increased neutrophils and growth of a pathogen in culture)

80
Q

What is the DDx for VAP?

A
Aspiration pneumonitis
PE with infarction
ARDS
Pulmonary hemorrhage
Lung contusion
Infiltrative tumour
Radiation pneumoniitis
Drug reaction
Cryptogenic organizing pneumonia
Vasculitis (eg SLE)
81
Q

What is the role of procalcitonin in VAP?

A

Suspected VAP: Conflicting evidence

Confirmed VAP: May be useful for discontinuing Abx and prognosis

82
Q

What factors, on top of risk factors for CAP, put pt at risk of VAP?

A

Biggest is mechanical ventilation (obviously)

Others: Chest or upper abdo surgery, agents that increase gastric pH, previous Abx exposure, reintubation or prolonged intubation, frequent vent circuit changes; many more

83
Q

What strategies can prevent aspiration in a ventilated pt?

A

Positioning: head of bed at 30-45 degrees
Subglottic draining (of secretions)
Gastric volume monitoring

84
Q

What GI intervention can prevent pneumonia in critically ill pt? How is it done?

A

Decontamination of digestive tract

  • oropharyngeal antiseptics (eg chlorhexidine)
  • selective decontamination (oropharyngeal non-absorbed Abx)
85
Q

How are stress-dose glucocorticoids used in critically ill pt?

A

Not clear; further study needed.

86
Q

What does the empiric regimen for HAP and VAP target?

A

Staphylococcus aureus, Pseudomonas aeruginosa, and other gram-negative bacilli.

87
Q

When should a pt with HAP/VAP be reassessed and considered for discontinuing or narrowing Abx therapy?

A

48 to 72 hours after the initiation of therapy

88
Q

What are the risk factors for MDR pathogens in pt with VAP?

A
  • IV antibiotic use within the previous 90 days
  • Septic shock at the time of VAP
  • ARDS preceding VAP
  • ≥5 days of hospitalization prior to the occurrence of VAP
  • Acute renal replacement therapy prior to VAP onset
89
Q

What is an appropriate empiric therapy for VAP with no MDR risk factors (when local biogram is not resistant)?

A

Any of:
Piperacillin-tazobactam 4.5 g IV q6h
Cefepime 2 g IV q8h
Levofloxacin 750 mg IV daily

90
Q

What regimen should pt with MDR risk factors get?

A

2 agents active against P. aeruginosa & other gram-negative
+
1 agent active against MRSA

91
Q

Name 5 Abx regimens active against P. aeruginosa & other gram-negative, appropriate for pt with MDR risk factors (6 listed)

A
Piperacillin-tazobactam 4.5 g IV q6h
Cefepime 2 g IV q8h
Ceftazidime 2 g IV q8h
Imipenem 500 mg IV q6h
Meropenem 1 g IV q8h
Aztreonam 2 g IV q8h

(This may be more niche than I really need to know?)

92
Q

Name 3 aminoglycosides

A

Amikacin 15 to 20 mg/kg IV daily

Gentamicin 5 to 7 mg/kg IV daily

Tobramycin 5 to 7 mg/kg IV daily

93
Q

Why should aminoglycosides be used cautiously, and discontinued if possible?

A
  • poor lung penetration
  • increased risk of nephrotoxicity and ototoxicity
  • poorer clinical response rates compared with other antibiotic classes

UpToDate discontinues adjunctive aminoglycosides after 48h if pt is clinically improving

94
Q

What should you do if you have a pt with VAP and you need to decide on an Abx regimen?

A

Look it up: will vary with

  • local antibiogram
  • suspected pathogens (eg legionella)
  • time, probably (ie not worth memorizing)
95
Q

If a pt is clinically improving 48-72h after starting treatment for S. aureus or MDR pathogens, what should you do?

A

If these pathogens are not grown in culture, d/c agents

96
Q

What should you do if a pt isn’t improving after being on Abx for 72h?

A

Evaluate for complications, other sites of infection, and alternate diagnoses

97
Q

How long do you keep a pt on Abx for HAP or VAP?

A

7d

98
Q

Name 3 toxicities of fluoroquinolones

A

QT interval prolongation, tendinitis and tendon rupture, and neurotoxicity.

99
Q

What toxicity is seen in polymyxins?

A

Nephrotoxicity

100
Q

What toxicity is associated with the combination of vancomycin and pip-tazo?

A

AKI

101
Q

What adverse event is seen in pt with renal insufficiency on imipenem and cefepime?

A

Seizure

102
Q

What is the goal of combination therapy in HAP and VAP?

A

Ensure that at least one active agent is administered as soon as possible in patients at risk for multidrug-resistant (MDR) pathogens

(during the empiric treatment phase before the infecting pathogen(s) has been identified and susceptibilities reported)

103
Q

What variables are associated with increased mortality in VAP and HAP?

A
  • Serious illness at the time of diagnosis (eg, high APACHE score, shock, coma, respiratory failure, ARDS)
  • Bacteremia
  • Severe underlying comorbid disease
  • Infection caused by an organism associated with multidrug resistance
  • Multilobar, cavitating, or rapidly progressive infiltrates on lung imaging
  • Delay in the institution of effective antimicrobial therapy
104
Q

What two things are required to produce aspiration pneumonia?

A

1) Compromise in the usual defenses that protect the lower airways (eg glottic closure, cough reflex, other clearing mechanisms)

2) One of:
- An inoculum deleterious to the lower airways by a direct toxic effect (such as gastric acid)
- stimulation of an inflammatory process from bacterial infection
- obstruction due to uncleared fluid or particulate matter

105
Q

What risk factors increase risk of aspiration pneumonia specifically? (over 5 listed)

A
  • reduced LOC
  • Dysphagia
  • Disorders of upper GI tract (esophageal disease, surgery, reflux)
  • mechanical disruption of glottic closure: trachostomy, ET intubation, bronchoscopy, endoscopy, NG feeding
  • pharyngeal anesthesia

Other misc: protracted vomiting, large-volume tube feedings, feeding gastrostomy, the recumbent position, and drowning

106
Q

What should be done for pt with observed aspiration?

A

Immediate tracheal suction to clear fluids and particulate matter that may cause obstruction

This maneuver will not protect the lungs from chemical injury, which occurs instantly

107
Q

What are the categories/syndromes of aspiration pneumonia?

A

chemical pneumonitis
bacterial infection
airway obstruction

108
Q

What are the more modifiable risk factors for CAP?

A
  • Smoking, EtOH, opioid
  • crowded living conditions
  • “residence in low-income settings”
  • environmental toxins