Hepatitis C

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Pneumonia
By Nicole Smidt Sarah Nainggolan
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Types of Pneumonia
1. Community-acquired (CAP) 2. Hospital-acquired
(nosocomial) (HAP) 3. Ventilator-associated (VAP)
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(CAP) Pathophysiology
-CAP is acquired by the body via an inhalational
or aspirational route. -Sometimes, CAP can be
obtained as a secondary bacteremia from another
part of the body resulting in pneumonia caused by
bacteria common to other areas of the body. -CAP
tends to affect the elderly, immunocompromised,
and those with underlying lung conditions (i.e.
COPD, chronic bronchitis).
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HP in a (CAP) patient

• History
• Varying degrees of fever with acute onset
• Productive cough with yellow/green sputum
• Pleuritic chest pain
• SOB

• Physical
• Auscultation of rales over the involved lobe or
  segment
• Increased tactile vocal fremitus, bronchial
  breathing, and egophony (egta sound)
• Purulent sputum
• Blood-tinged sputum
• Signs of consolidation

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Bacterial Pathogens of (CAP) 85 of CAPs

• Streptococcus pneumoniae
• MCC
• H. influenzae
• - COPD
• Moraxella catarrhalis
• MC in patients with chronic bronchitis COPD

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Common Pathogens/Atypical Hosts
-Staph aureus causes CAP in the setting of
postviral influenza. -Klebsiella pneumoniae
causes CAP in chronic alcoholics. Aspiration
pneumonia is typically caused by multiple
pathogens. -Pseudomonas aeruginosa is a cause of
CAP in patients with cystic fibrosis and
bronchiectasis.
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Atypical Pathogens of CAP

• Zoonotic
• Chlamydia psittaci
• Psittacosis
• Recent close contact with birds
• Francisella tularensis
• Tularemia
• Contact with deer or rabbits or recent bite by a
  tick or deer fly
• Coxiella burnetii
• Q fever
• Contact with a cat or sheep that has given birth
  recently

• Non-zoonotic
• (15 of CAPs)
• Legionella
• Elderly, smokers,
• immunocompromised
• Mycoplasma pneumoniae
• Young and healthy
• Chlamydia pneumoniae
• Young healthy

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Atypical CAP
-Atypical pneumonias commonly present with dry
cough, extrapulmonary involvement, and patchy
interstitial pattern on CXR.
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Differential Dx of CAP
-Chronic bronchitis -Myocardial
infarction -Asthma -CHF -Pulmonary
edema -PE -Acute hypersensitivity
reaction -Bronchogenic carcinoma
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Laboratory Studies of CAP
-CBC with differential showing a neutrophilia
w/left shift, electrolytes, elevated BUN/Cr,
elevated glucose, abnormal LFTs -Sputum Gram
stain and/or culture (should have lt10 squamous
cells/lpf/purulent should have gt25 PMNs/lpf) -2-3
sets of blood cultures (before antibiotics) to
detect presence of bacteria in the blood -Serum
cold agglutinin titers (Mycoplasma) -Urinalysis -S
erological testing if zoonotic atypical pathogens
are suspected
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Imaging Studies of CAP
-Chest x-ray Repeat chest x-ray within 24 hours
if first x-ray shows negative findings with high
clinical suspicion -Serial chest x-rays to
observe for progression or check for
resolution -Chest CT scan If failing to
respond to therapy
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Community Acquired Pneumonia (CAP) Treatment

• Decision to hospitalize
• Pneumonia Severity Index (PSI)
• Points given for 20 variables i.e. age, comorbid
  conditions, abnormal PE lab findings
• Add up the points patients are categorized into
  5 classes

Total points Risk Class Mortality Treat as
No predictors I 0.1 Outpatient
70 II 0.6 Outpatient
71-90 III 2.8 Inpatient, briefly
91-130 IV 8.2 Inpatient
gt130 V 29.2 Inpatient
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Decision to hospitalize, cont.

• 2. CURB-65
• Five variables
• CConfusion
• UUrea gt 7mmol/L
• RRespiratory rate 30
• BBP systolic 90, diastolic 60
• Age 65
• Add up the points, patients are categorized into
  3 classes

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Decision to hospitalize, cont.

• CURB-65, cont.
• PSI-less practical
• CURB-65-less studies done

Total points 30-day Mortality Risk Treat as
0 1.5 Outpatient
1-2 9.2 Inpatient
3 22 ICU
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CAP Treatment

• Empiric antibiotic treatment
• Outpatient treatment
• Previously healthy or no antibiotics in last 3
  months
• Comorbidities or antibiotics in last 3 months
• Inpatient treatment
• Non-ICU patients
• ICU patients

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CAP TreatmentOutpatient antibiotics Guidelines
per IDSA and ATS
Previously healthy/no antibiotics in last 3 months Comorbidities/antibiotics in last 3 months
Clarithromycin 500 mg PO BID, or Levofloxacin 750 mg PO QD, or moxifloxacin 400 mg PO QD, or gemifloxacin 320 mg PO QD, OR
Azithromycin 500 mg PO once, then 250 mg PO QD, or Amoxicillin 1g TID, or Amoxicillin/clavulanate 2g BID, or
Doxycycline 100 mg PO BID Ceftriaxone 1-2g IV QD, cefpodoxime 200 mg PO BID, cefuroxime 500 mg PO BID , plus a macrolide
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CAP TreatmentInpatient Antibiotics
Inpatient, non-ICU Inpatient, ICU
Levofloxacin 750 mg PO or IV QD, or moxifloxacin 400 mg PO or IV QD, or gemifloxacin 320 mg PO QD Cefotaxime 12 g IV q8h, or ceftriaxone 2 g IV QD, or ampicillin-sulbactam 2 g IV q8h plus azithromycin or a fluoroquinolone PCN-allergic use resp. fluoroquinolone and aztreonam 2 g IV q8h
Cefotaxime 12 g IV q8h, or ceftriaxone 12 g IV QD, or ampicillin 12 g IV q46h, or ertapenem 1 g IV qd in selected patients plus a macrolide (oral clarithromycin or azithromycin or IV azithromycin 1 g once, then 500 mg QD) PCN-allergic use resp. fluroquinolones
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CAP Treatment Special Considerations

• Pseudomonas
• piperacillin/tazobactam 4.5 g IV q6h, cefepime
  12 g IV q12h, imipenem 500 mg IV q6h, meropenem
  1 g IV q8h plus either ciprofloxacin 400 mg IV
  q12h or levofloxacin 750 mg IV, or
• piperacillin/tazobactam 4.5 g IV q6h plus
  amikacin 15 mg/kg qd or tobramycin 1.7 mg/kg qd
  and azithromycin, or
• piperacillin/tazobactam 4.5 g IV q6h plus an
  aminoglycoside plus an antipneumococcal
  fluoroquinolone
• If PCN-allergic substitute aztreonam

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CAP TreatmentSpecial Considerations

• Community-Acquired MRSA
• Add linezolid 600 mg IV q12h or vancomycin 1 g IV
  q12h

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CAP Treatment

• Most patients admitted to the hospital for CAP
  receive IV antibiotics
• A switch to oral drugs is appropriate, so long as
  the patient can ingest and absorb the drugs, is
  hemodynamically stable, and showing clinical
  improvement
• Duration Patients are usually treated for 10-14
  days, but recent studies with fluoroquinolones
  suggest that a 5-day course is sufficient for
  uncomplicated CAP.

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CAPFollow-up

• Fever usually resolves within 2 days, while
  leukocytosis may improve within 4 days
• Abnormalities in CXR take 4-12 weeks to clear,
  depending on the age of the patient and the
  underlying lung disease
• Follow-up CXR can be done 4-6 weeks later
• If recurrence is seen in the same lung segment,
  possible neoplasm should be taken into
  consideration

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CAPPrognosis

• Depends on age, comorbidities, inpatient/outpatien
  t
• Young patients without comorbidities fully
  recover in 2 weeks
• Older patients with comorbidities take longer
• Overall mortality rates
• Outpatient lt 1
• Inpatient 10, with about 50 of the deaths
  directly attributable to pneumonia

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Healthcare-associated Pneumonia
1. Hospital-acquired pneumonia (HAP) 2.
Ventilator-associated pneumonia (VAP) The main
difference from CAP significantly lower
incidence of atypical pathogens, EXCEPT
Legionella
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Hospital-acquired pneumonia (HAP)
Defined as pneumonia that occurs more than 48
hours after admission but that was NOT incubating
at the time of admission. The American Thoracic
Society further subdivides nosocomial pneumonia
into early (occurring within the first 4 days of
hospitalization) and late (occurring after the
5th day of admission) onset.
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HAP Pathophysiology
-HAP is primarily acquired though aspiration of
oropharyngeal secretions into the
trachea. -Although uncommon, hematogenous spread
is also possible. -HAP is mainly caused by
aerobic gram-negative bacilli of two forms
necrotizing and nonnecrotizing. Necrotizing
cause rapid cavitation, microabscess formation,
blood-vessel invasion, and hemorrhage (i.e. P.
aeruginosa).
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HAP
-Usually bacterial in nature. -Common in patients
with mechanical ventilation as intubation and
ventilation support bypass the normal host
defense mechanisms. -One of the most common
diagnoses in the medical and surgical ICUs.
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HP of HAP
History -SOB -Productive cough -Fever
Physical -Rales on auscultation over affected
area -Generally NO consolidation in nosocomial
pneumonia
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HAP Microbiology
-P. aeruginosa -Klebsiella -E. coli -Acinetobact
er (common in ICU patients) -Staph aureus -Strep
pneumoniae -H. influenzae
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Dx of HAP
Laboratory -White blood cell count -Blood
cultures
Imaging Studies -Serial chest x-rays to check
for progression and resolution -CT or spiral CT
scan
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Hospital-acquired Pneumonia (HAP)

• Main differences from VAP
• Lower incidence of MDR pathogens (allows more
  monotherapy)
• Better host immunity
• Anaerobes are more common
• Specific therapy aimed at anaerobes is not
  indicated, unless aspiration is a concern
• Lower risk of antibiotic failure in comparison to
  VAP
• Lower mortality rates than VAP

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Ventilator-associated pneumonia
Defined as pneumonia that develops 48 hours or
longer after mechanical ventilation is given via
endotracheal tube or tracheostomy.
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VAP Pathophysiology
-VAP is caused by invasion of the lower
respiratory tract and lung tissue by
microorganisms caused by decreased integrity of
the oropharynx and trachea allowing oral and
gastric sections to enter. -The incidence of VAP
increases with the duration of ventilation.
-Pseudomonas and Acinetobacter pneumonia is
associated with the greatest mortality.
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Dx of VAP
History 1. Hospitalization of greater than 5
days 2. Hospital admission of more than 2 days in
the last 90 days 3. Antibiotic use in the last 90
days 4. Residing in a nursing home or skilled
care facility 5. Home infusion therapy or wound
care 6. Dialysis within the last 30 days 7.
Immunocompromised
Diagnostic Triad 1. Fever 2. Purulent
secretions 3. Leukocytosis
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Work-up of VAP
-CBC with differential to evaluate white blood
cell count -Routine blood tests to assess
patient's baseline renal and hepatic function to
properly dose antibiotics -Blood
cultures -Respiratory secretion
cultures -Portable chest radiography -Air
bronchogram
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Ventilator-associated Pneumonia (VAP)

• Empirical Antibiotic Treatment

Patients with NO risk factors for MDR pathogens Patients with risk factors for MDR pathogens
Ceftriaxone 2 g IV q24h, or 1. Ceftazidime 2 g IV q8h or cefepime 2 g IV q812h, or
Moxifloxacin 400 mg IV q24h, ciprofloxacin 400 mg IV q8h, or levofloxacin 750 mg IV q24h, or Piperacillin/tazobactam 4.5 g IV q6h, imipenem 500 mg IV q6h or 1 g IV q8h, or meropenem 1 g IV q8h, plus
Ampicillin/sulbactam 3 g IV q6h, or 2. Gentamicin or tobramycin 7 mg/kg IV q24h or amikacin 20 mg/kg IV q24h or Ciprofloxacin 400 mg IV q8h or levofloxacin 750 mg IV q24h, plus
Ertapenem 1 g IV q24h 3. Linezolid 600 mg IV q12h or Vancomycin 15 mg/kg, up to 1 g IV, q12h
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VAP Treatment

• Duration 8 days (associated with less frequent
  emergence of antibiotic-resistant strains)
• Pseudomonas aeruginosa causes high rates of
  clinical failure and death, despite combo therapy
• VAP caused by MRSA 40 clinical failure rate
  when treated with standard-dose vancomycin, so
  treat with linezolid instead.

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VAPFollow-up

• Clinical improvement is usually seen within 48-72
  hours following initial antibiotic therapy
• CXR worsens during initial treatment, so less
  helpful
• In very ill patients, follow-up CXR can be done
  every few days
• Once patient has improved, CXR may not be
  necessary for a few weeks

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VAPPrognosis

• Associated with high crude mortality rates
  (50-70)
• Stenotrophomonas maltophilia prognosis is very
  poor (death is almost inevitable)

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Question 1 From USMLEWORLD

• A 65-year-old white male who has a history of
  COPD, CHF, and CAD presented with a three-day
  history of worsening SOB, cough with yellowish
  expectoration, and fever. He is not on steroids
  and does not use oxygen at home. He takes
  ipratropium, albuterol, aspirin, digoxin,
  furosemide, metoprolol, and lisinopril. He lives
  at home with his wife. His temp is 103 F, BP is
  110/70, pulse is 110, and respirations are 24. He
  is saturating 88 on room air. He was started on
  3-liters of oxygen to keep the saturations above
  92. The CXR of the patient is shown below. What
  is the most appropriate next step in the
  management of this patient?
• A. Admit the patient and give ampicillin
• B. Outpatient trimethoprim-sulfamethoxazole
• C. Admit the patient and start levofloxacin
• D. Admit the patient and start ciprofloxacin
• E. Admit the patient and start vancomycin
• F. Outpatient clindamycin therapy

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Question 1 CXR

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Answer 1

• C. Admit the patient and start levofloxacin
• The clinical presentation and CXR of this patient
  is highly suggestive of CAP. The first step in
  the management of CAP is to decide whether the
  patient needs hospitalization. The decision to
  admit the patient is generally made using the
  Pneumonia Severity Index (PSI) based on medical
  history, PE, and lab and radiographic findings.
  This patient has other comorbidities such as CHF,
  COPD, and CAD, and his oxygen saturation is less
  than 90. Thus he falls under risk class III or
  IV and needs to be hospitalized.
• The most common cause of lobar pneumonia in this
  setting is pneumococcus. The new generation
  flouroquinolones (i.e. levofloxacin) is used for
  the inpatient treatment of CAP. About 97 of the
  Streptococcus pneumonia are sensitive to these
  drugs. They also cover the atypical organisms.
• For the management of outpatient therapy in
  stable patients with no comorbidities, either
  azithromycin or doxycycline can be used.

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Question 2
A 68-year-old woman with polymyositis is
evaluated in the office because of increased
difficulty swallowing and a 2-week history of
low-grade fever, intermittent cough, and sputum
production. On physical examination, temperature
is 37.9 C (100.2 F), and crackles are heard at
the base of the right lung posteriorly. The
leukocyte count is 9700/µL with 85 neutrophils,
12 lymphocytes, 2 monocytes, and 1
eosinophils. A chest radiograph shows patchy
pulmonary infiltrates in the right lower lobe.
Sputum Gram stain shows many neutrophils, a few
squamous epithelial cells, and several
morphologic types of both gram-negative rods and
gram-positive cocci. Results of sputum culture
are pending. Which of the following is the most
appropriate management at this time? A.
Bronchoscopy B. Clindamycin C. Metronidazole D.
Penicillin
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Answer 2
B. This patient should be started on clindamycin.
The presence of underlying polymyositis and
difficulty swallowing place this patient at risk
for aspiration and the development of aspiration
pneumonia. Other risk factors for aspiration
pneumonia include episodes of depressed
consciousness (e.g., patients with alcoholism) or
mechanical factors that increase the likelihood
of secretions entering the tracheobronchial tree
(e.g., patients with esophageal obstruction).
Although aspiration of acidic gastric contents
can result in a chemical pneumonitis, aspiration
of oral secretions typically results in an
anaerobic pneumonia caused by anaerobic organisms
that are normally present in the mouth. A sputum
Gram stain often shows both gram-positive and
gram-negative organisms of different morphologic
types, as was found in this patient. The typical
location of aspiration pneumonia depends upon the
patient's position at the time of aspiration.
Based on gravitational flow of airway secretions,
the pneumonia is preferentially localized in the
dependent regions of the lung at the time of
aspiration. In an upright patient, the lower
lobes are usually affected, more so on the right
than on the left. In a supine patient, common
sites of aspiration pneumonia are the posterior
segment of the right upper lobe and the superior
segment of the right lower lobe. Although
options for antibiotic coverage of anaerobic
aspiration pneumonia have generally included
either penicillin or clindamycin, controlled
studies have shown that antibiotic failure rates
have been higher for penicillin than for
clindamycin. Metronidazole does not adequately
cover microaerophilic and aerobic streptococci
from the mouth, which are contributing organisms
in many patients with aspiration pneumonia.
Bronchoscopy is not indicated because it is
unable to confirm anaerobic infection, since
anaerobic organisms from the mouth will
contaminate the specimens obtained.
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References

• Mandell LA, Wunderick R, et al. Harrisons
  Principles of Internal Medicine, 17th ed. 2008.
• Chesnutt MS, Gifford AH, Prendergast TJ. Current
  Medical Diagnosis Treatment 2010.
• Agabegi SS, Agabegi ED. Step-Up to Medicine, 2nd
  ed. 2008.
• Fischer C, Reichert S. USMLE Master the Boards.
  2009.
• Burke A Cunha, MD. Emedicine.medscape.com. 2010.