Community-Acquired

Pneumonia
Joanna M. Delaney, D.O.
Georgetown University /
Providence Hospital
June 8, 2007
Objectives
Describe the common pathogenesis and
pathogens of pneumonia
Discuss diagnosis and initial management of
community acquired pneumonia (CAP)
Understand features of the Pneumonia PORT
Severity Index
Discuss the IDSA/ATS guidelines and
recommendations for final antibiotic choice
Understand issues in basic management for
pneumonia in children, nursing home patients,
and immunocompromised patients.
Epidemiology
Unclear! Few population-based statistics on the
condition alone
CDC combines PNA with influenza for morbidity
& mortality data
PNA & influenza = 7th leading causes of death in the
US (2001)
Age-adjusted death rate = 21.8 per 100,000
Mortality rate: 1-5% out-Pt, 12% In-Pt, 40% ICU
Death rates increase with comorbidity and age
Affects race and sex equally

Community Acquired
Pneumonia
Infection of the lung parenchyma in a
person who is not hospitalized or living
in a long-term care facility for 2 weeks
5.6 million cases annually in the U.S.
Estimated total annual cost of health care
= $8.4 billion
Most common pathogen = S. pneumo (60-
70% of CAP cases)

Nosocomial Pneumonia
Hospital-acquired pneumonia (HAP)
Occurs 48 hours or more after admission,
which was not incubating at the time of
admission
Ventilator-associated pneumonia (VAP)
Arises more than 48-72 hours after
endotracheal intubation
Nosocomial Pneumonia
Healthcare-associated pneumonia (HCAP)
Patients who were hospitalized in an acute care
hospital for two or more days within 90 days of the
infection; resided in a nursing home or LTC facility;
received recent IV abx, chemotherapy, or wound care
within the past 30 days of the current infection; or
attended a hospital or hemodialysis clinic
Guidelines for the Management of Adults with
HAP, VAP, and HCAP. American Thoracic
Society, 2005
Pathogenesis
Inhalation, aspiration and hematogenous
spread are the 3 main mechanisms by
which bacteria reaches the lungs
Primary inhalation: when organisms
bypass normal respiratory defense
mechanisms or when the Pt inhales
aerobic GN organisms that colonize the
upper respiratory tract or respiratory
support equipment
Pathogenesis
Aspiration: occurs when the Pt aspirates
colonized upper respiratory tract
secretions
Stomach: reservoir of GNR that can ascend,
colonizing the respiratory tract.
Hematogenous: originate from a distant
source and reach the lungs via the blood
stream.
Pathogens
CAP usually caused by a single organism
Even with extensive diagnostic testing,
most investigators cannot identify a
specific etiology for CAP in 50% of
patients.
In those identified, S. pneumo is causative
pathogen 60-70% of the time

Streptococcus pneumonia
Most common cause of CAP
Gram positive diplococci
Typical symptoms (e.g. malaise, shaking
chills, fever, rusty sputum, pleuritic hest
pain, cough)
Lobar infiltrate on CXR
Suppressed host
25% bacteremic
Atypical Pneumonia
#2 cause (especially in younger population)
Commonly associated with milder Sxs:
subacute onset, non-productive cough, no focal
infiltrate on CXR
Mycoplasma: younger Pts, extra-pulm Sxs
(anemia, rashes), headache, sore throat
Chlamydia: year round, URI Sx, sore throat
Legionella: higher mortality rate, water-borne
outbreaks, hyponatremia, diarrhea
Pneumonia
Viral Pneumonia
More common cause in children
RSV, influenza, parainfluenza
Influenza most important viral cause in
adults, especially during winter months
Post-influenza pneumonia (secondary
bacterial infection)
S. pneumo, Staph aureus

Other bacteria
Anaerobes
Aspiration-prone Pt, putrid sputum, dental disease
Gram negative
Klebsiella - alcoholics
Branhamella catarrhalis - sinus disease, otitis, COPD
H. influenza
Staphylococcus aureus
IVDU, skin disease, foreign bodies (catheters,
prosthetic joints) prior viral pneumonia
Diagnosis and Management
Guidelines
American Thoracic Society
Guidelines for the Management of Adults with CA
(2001)
Infectious Diseases Society of America
Update of Practice Guidelines for the Management of
CAP in Immunocompetent adults (2003)
ATS and IDSA joint effort
IDSA/ATS Consensus Guidelines on the
Management of CAP in Adults (March 2007)
Guidelines
2001 ATS & 2003 IDSA Guideline Update
Expert panels
Evidence-based recommendations
Recommend patient stratification to
identify likely pathogens and suggested
empiric abx
Site of care
Presence of cardiopulmonary disease
Presence of modifying factors
Clinical Diagnosis
Suggestive signs and symptoms
CXR or other imaging technique
Microbiologic testing

Signs and Symptoms
Fever or hypothermia
Cough with or without sputum, hemoptysis
Pleuritic chest pain
Myalgia, malaise, fatigue
GI symptoms
Dyspnea
Rales, rhonchi, wheezing
Egophony, bronchial breath sounds
Dullness to percussion
Atypical Sxs in older patients
Clinical Diagnosis: CXR
Demonstrable infiltrate by CXR or other
imaging technique
Establish Dx and presence of complications
(pleural effusion, multilobar disease)
May not be possible in some outpatient
settings
CXR: classically thought of as the gold
standard

Infiltrate Patterns
Pattern Possible Diagnosis
Lobar S. pneumo, Kleb, H. flu,
GN
Patchy Atypicals, viral,
Legionella
Interstitial Viral, PCP, Legionella
Cavitary Anaerobes, Kleb, TB, S.
aureus, fungi
Large effusion Staph, anaerobes, Kleb
Clinical Diagnosis:
Recommended testing
Outpatient: CXR, sputum Cx and Gram
stain not required (broaden initial AB tx)
Inpatient: CXR, Pox or ABG, chemistry,
CBC, two sets of blood Cxs
If suspect drug-resistant pathogen or
organism not covered by usual empiric abx,
obtain sputum Cx and Gram stain.
Severe CAP: Legionella urinary antigen,
consider bronchoscopy to identify pathogen
Clinical Diagnosis
Assess overall clinical picture
PORT Pneumonia Severity Index (PSI)
Aids in assessment of mortality risk and
disposition
Age, gender, NH, co-morbidities, physical
exam lab/radiographic findingsHospital
Admission Decision
CURB-65 criteria (confusion, uremia, RR,
low BP, age 65 yrs or greater) or PSI can
be used to ID candidates for outpt
management



IDSA: Outpt Management in
Previously Healthy Pt
Organisms: S. pneumo, Mycoplasma, viral,
Chlamydia pneumo, H. flu
Recommended abx:
Advanced generation macrolide (azithro or clarithro)
or doxycycline
If abx within past 3 months:
Respiratory quinolone (moxi-, levo-, gemi-), OR
Advanced macrolide + amoxicillin, OR
Advanced macrolide + amoxicillin-clavulanate
IDSA: Outpt Management in
Pt with comorbidities
Comorbidities: cardiopulmonary dz or
immunocompromised state
Organisms: S. pneumo, viral, H. flu, aerobic GN
rods, S. aureus
Recommended Abx:
Respiratory quinolone, OR advanced macrolide
Recent Abx:
Respiratory quinolone OR
Advanced macrolide + beta-lactam
IDSA: Inpt Management-
Medical Ward
Organisms: all of the above plus polymicrobial
infections (+/- anaerobes), Legionella
Recommended Parenteral Abx:
Respiratory fluoroquinolone, OR
Advanced macrolide plus a beta-lactam
Recent Abx:
As above. Regimen selected will depend on nature of
recent antibiotic therapy.

IDSA: Inpt Management-
Severe/ICU
One of two major criteria:
Mechanical ventilation
Septic shock, OR
Two of three minor criteria:
SBP90mmHg,
Multilobar disease
PaO2/FIO2 ratio < 250
Organisms: S. pneumo, Legionella, GN,
Mycoplasma, viral, ?Pseudomonas
IDSA: Inpt Management:
Severe/ICU
No risk for Pseudomonas
IV beta-lactam plus either
IV macrolide, OR IV fluoroquinolone
Risk for Pseudomonas
Double therapy: selected IV antipseudomonal beta-
lactam (cefepine, imipenem, meropenem,
piperacillin/tazobactam), plus
IV antipseudomonal quinolone
-OR-
Triple therapy: selected IV antipseudomonal beta-
lactam plus
IV aminoglycoside plus either
IV macrolide, OR IV antipseudomonal quinolone
Switch to Oral Therapy
Four criteria:
Improvement in cough and dyspnea
Afebrile on two occasions 8 h apart
WBC decreasing
Functioning GI tract with adequate oral intake
If overall clinical picture is otherwise
favorable, can can switch to oral therapy
while still febrile.
Prevention
Smoking cessation
Vaccination per ACIP recommendations
Influenza
Inactivated vaccine for people >50 yo, those at risk
for influenza compolications, household contacts of
high-risk persons and healthcare workers
Intranasal live, attenuated vaccine: 5-49yo without
chronic underlying dz
Pneumococcal
Immunocompetent 65 yo, chronic illness and
immunocompromised 64 yo
Pneumonia in the Elderly
Prevention important
Presentation can be subtle
Antibiotic choice in CAP is same as other adults
Healthcare associated pneumonia
Consider S. aureus (skin wounds) and GN bacteria
(aspiration)

Pneumonia in Older Residents of Long-term Care Facilities.
AFP 2004; 70: 1495-1500.
Pneumonia in
Immunocompromised Pts
Smokers, alcoholics, bedridden, immuno-
compromised, elderly
Common still common
S. pneumo
Mycoplasma
Pneumocystis Carinii Pneumonia
P. jirovecii
Fever, dyspnea, non-prod cough (triad 50%),
insidious onset in AIDS, acute in other
immunocompromised Pts
CXR: bilateral interstitial infiltrates
Steroids for hypoxia
TMP-SMZ still first line
IDSA/ATS 2007 Guideline
Hospital Admission Decision
CURB-65 criteria (confusion, uremia, RR, low BP,
age 65 yrs or greater) or PSI can be used to ID
candidates for outpt management
Diagnostic Testing
Acknowledges the low yield and infrequent positive
impact on clinical care
Outpt testing for etiologic Dx remain optional
Inpt testing for etiologic Dx recommended for specific
indications
Antimicrobial therapy: essentially unchanged

Summary
Use overall clinical presentation to guide
therapy
The admission decision is an art of
medicine decision
Use risk factors and guidelines to assist
with clinical judgement
References
American Thoracic Society. Guidelines for the Management of
Adults with Community-acquired Pneumonia. Am J Respir Crit
Care Med 2001 Vol. 163:1730-1754.

Mandell LA, Bartlett JG, Dowell SF, File TM Jr, Musher DM,
Whitney C. Update of practice guidelines for the management of
community-acquired pneumonia in immunocompetent adults. Clin
Infect Dis 2003 Dec 1;37(11):1405-33.

Mandell LA, Wunderink RG, Anzueto A, Bartlett JG, Campbell
GD, Dean NC, Dowell SF, File TM Jr, Musher DM, Niederman
MS, Torres A, Whitney CG. Infectious Diseases Society of
America/American Thoracic Society consensus guidelines on the
management of community-acquired pneumonia in adults. Clin
Infect Dis 2007 Mar 1;44 Suppl 2:S27-72.

Arch Ped Adol Med 1995; 149: 283-7.
Nosocomial
Pneumonia
Definition
Nosocomial pneumonia:

Occurring at least 48 hours after admission
and not incubating at the time of
hospitalization
Introduction
Nosocomial pneumonia is the 2
nd
most
common hospital-acquired infections after UTI.
Accounting for 31 % of all nosocomial infections

Nosocomial pneumonia is the leading cause of
death from hospital-acquired infections.

The incidence of nosocomial pneumonia is
highest in ICU.
Introduction
The incidence of nosocomial pneumonia in
ventilated patients was 10-fold higher than non-
ventilated patients

The reported crude mortality for HAP is 30% to
greater than 70%.

--- Medical Clinics of North America
Therapy of Nosocomial pneumonia 2001 vol.85 1583-94
Pathogenesis
Pathogenesis
For pneumonia to occur, at least one of the
following three conditions must occur:

1. Significant impairment of host defenses
2. Introduction of a sufficient-size inoculum to overwhelm
the host's lower respiratory tract defenses
3. The introduction of highly virulent organisms into the
lower respiratory tract
Most common is microaspiration of
oropharyngeal secretions colonized with
pathogenic bacteria.
Pathogenesis
--- The Prevention of Ventilator-Associated Pneumonia Vol.340 Feb 25, 1999 NEJM
Classification
Early-onset nosocomial pneumonia:
Occurs during the first 4 days
Usually is due to S. pneumoniae, MSSA, H. Influenza,
or anaerobes.
Late-onset nosocomial pneumonia:
More than 4 days
More commonly by G(-) organisms, esp. P. aeruginosa,
Acinetobacter, Enterobacteriaceae (klebsiella,
Enterobacter, Serratia) or MRSA.
Causative Agent
Enteric G(-) bacilli are isolated most
frequently particularly in patients with late-
onset disease and in patients with serious
underlying disease often already on broad-
spectrum antibiotics.

Prior use of broad-spectrum antibiotics and
an immunocompromised state make resistant
gram-negative organisms more likely.
Causative Agent

P. aeruginosa and Acinetobacter are common
causes of late-onset pneumonia, particularly in
the ventilated patients.

Causative Agent
S. aureus is isolated in about 20~40% of
cases and is particularly common in :
1. Ventilated patients after head trauma, neurosurgery,
and wound infection
2. In patients who had received prior antibiotics or
Prolonged care in ICU

MRSA is seen more commonly in patients
Received corticosteroids
Undergone mechanical ventilation >5 days
Presented with chronic lung disease
Had prior antibiotics therapy
Causative Agent
Anaerobes are common in patients
predisposed to aspiration

VAP with anaerobes occurred more often with
oropharyngeal intubation than nasopharyngeal
intubation.
Causative Agent
Legionella pneumophilia occurs sporadically but may
be endemic in hospitals with contaminated water
systems. The incidence is underestimated because the
test to identify Legionella are not performed routinely.

Because the incubation period of Legionella infection is
2 to 10 days. cases that occur more than 10 days after
admission are considered to be nosocomial, and cases
that develop between 4 and 10 days are considered as
possible nosocomial.

Patients who are immunocompromised, critically ill, or
on steroids are at highest risk for infection.
Ventilator-associated
Pneumonia (VAP)
Ventilator-associated
Pneumonia (VAP)
Definition:
Nosocomial pneumonia has developed in patient who
are receiving mechanical ventilation

Classification:
Early-onset: within 48-72 hours after tracheal
intubation, which complicates the
intubation process
Late-onset: after 72 hours
Pathogenesis
Require 2 important processes:
1. Bacterial colonization of the aerodigestive tract
2. Aspiration of contaminated secretion into the
Lower airway

Prevents mechanical clearance by cough and
the mucociliary escalator.
Prevention for VAP
The oral regimen (topical gentamicin, Colistin,
Vancomycin cream q6h for 3 weeks) treating
oropharyngeal colonization could prevent VAP.


--- Prevention of VAP by oral decontamination
American journal of respiratory critical care medicine2001 164:382-8
Preventions for VAP
Non-pharmacologic strategies

Effective hand washing and use of protective gowns and
gloves
Semirecumbent positioning
Avoidance of large gastric volume
Oral (non-nasal) intubation
Continuous subglottic suctioning
Humidification with heat and moisture exchanger
Posture change
--- The Prevention of Ventilator-Associated Pneumonia Vol.340 Feb 25, 1999 NEJM
Preventions for VAP
Pharmacologic strategies

Stress-ulcer prophylaxis
Combination antibiotic therapy
Prophylactic antibiotic therapy
Chlorhexidine oral rinse
Prophylactic treatment of neutropenic pt
Vaccines
--- The Prevention of Ventilator-Associated Pneumonia Vol.340 Feb 25, 1999 NEJM
Treatment
Treatment
Most initial therapy is empiric because no
pathogen is identified or results are not available
when antimicrobial decisions are made in most
patients.
Treatment
Initially be treated with a broad-spectrum
antibiotic regimen aimed at covering all likely
bacterial pathogen

This regimen should subsequently be narrowed,
according to the result of culture
Treatment
The pathogen may be influenced by coexisting
illnesses, prior treatment, and length of
hospitalization.

The frequency of ICU-acquired P. Aeruginosa
carriage or colonization/infection was 23.4% at 7
days and 57.8% at 14 days.

---- Current opinion in infectious disease 2002, 15:387-94, copyright LWW
Treatment
The mortality can be reduced with early
appropriate empiric therapy.(Form 30 % with
appropriate therapy to more than 90 % with inappropriate therapy)

Inappropriate initial antibiotic therapy was
associated with:
1. Higher crude hospital mortality (60.7 vs. 47.3%)
2. Longer ICU stay in survivors (20 vs. 12 days)
3. Longer duration of mechanical ventilator

---- Current opinion in infectious disease 2002, 15:387-94, copyright LWW
Treatment
Guideline was published in 1996 by American
thoracic society and separated patients into
three groups, each with a set of probable
pathogens.

Group 1: mild to moderate HAP with no risk factor
Group 2: mild to moderate HAP with risk factor
Group 3a: severe HAP, early-onset with no risk factor
Group 3b: severe HAP, late-onset or with risk factor
Group 1. & 3a.
(Or 4th cephalosporin, Cefepime)
Group 2.
Group 3b.
prolonged ICU course
structural lung disease
previous antibiotic use
Treatment
For mild-to-moderate HAP, monotherapy has
been shown to be effective.

For severe HAP in which infection with resistant
organisms is likely, combination therapy
probably should be instituted until culture result
are available.
Treatment
Patients for S. aureus infection, agents against
this organism are necessary, including
Vancomycin if MRSA is suspected.

Linezolid is comparable with Vancomycin.
The advantage of Linezolid is less possible
nephrotoxicity

---- current opinion in infectious disease 2002, 15:387-94, copyright LWW
Treatment
Combination of antipseudomonal drugs is
controversial:
1. Traditional:
antipseudomonal beta-lactam with an Aminoglycoside.
Synergy but potential nephrotoxicity.
2. Another approach:
antipseudomonal beta-lactam with a Fluoroquinolone. No
benefit of synergy but reduce concern of nephrotoxicity, and
quinolone gets into the lungs at higher concentrations.
Treatment
Results:
1. Some pathogens, such as H. influenzae, cure
rate is high, and 7 to 10 days is adequate.

2. Highly resistant G(-) organisms (Acinetobacter or
pseudomonas) require prolonged combination
therapy for 21 days.

3. MRSA, requiring prolonged therapy.
Response of Therapy
Response of Therapy
Because of the delays in clinical response of treatment,
it is thought that unless there is significant clinical
deterioration or new microbiologic information, therapy
should not be changed for at least the first 48 to 72
hours

Measured by quantitating the bacterial load in the
lower respiratory tract at the initiation of therapy and
several days later.
Bacterial concentrations decreased or no growth -- clinical improvement
Elevated -- experienced clinical failure
Response to Therapy
If no clinical response is noted or deterioration occurs,
we need to consider:
1. Infectious causes:
Resistant pathogen
Superinfection
Unusual pathogens
Lung abscess
Extrapulmonary infection
2. Noninfectious events:
Heart: CHF
Lung: fibroproliferative ARDS, pulmonary emboli, Atelectasis
Reference
The prevention of ventilator-associated pneumonia
NEJM vol.340 Feb 25, 1999

Therapy of nosocomial pneumonia
Medical clinics of north America 2001 vol.85 1583-94

Prevention of VAP by oral decontamination
American journal of respiratory critical care medicine 2001 164:382-8

Current opinion in infectious disease
Copyright LWW 2002, 15:387-94


Thanks for Your
Attention!!
Aspiration Pneumonia
Aspiration
Defined as the inhalation of material into the airway
below the level of the true vocal cords
Two primary mechanisms of injury may ensue:
Aspiration pneumonitis non-infectious acute
inflammatory reaction characterized by infiltration on
radiography
Aspiration pneumonia parenchymal inflammatory
reaction to an infectious agent characterized by an
infiltrate on chest radiograph


McClave SA, DeMeo MT, DeLegge MH et al. North American summit on aspiration in the critical illpatient: consensus statement. Journal of
Parenteral and Enteral Nutrition; 6: S8085
Marom EM, McAdams HP, Erasmus JJ. The many faces of pulmonary aspiration. AJR Am Roentgenol. Jan 1999;172(1):121-8


Aspiration Pneumonitis
The chemical pneumonitis and lung injury was first
described by Mendelson in 1946.
Characterized by a biphasic injury pattern based on
animal models
Initial phase: peaks within 1 hour; increase in capillary
permeability secondary to direct chemical burn.
Second phase: peaks at 4 hours; acute inflammatory response
with infiltration of inflammatory mediators into lung interstitium
and alveoli.



Kennedy TP, Johnson KJ, Kunkel RG, Ward PA, Knight PR, Finch JS. Acute acid aspiration lung injury in the rat: biphasic
pathogenesis. Anesth Analg 1989;69:87-92

Aspiration Pneumonitis
Severity of lung injury is primarily based on three
factors; the pH, volume, and particulate nature
of aspirated contents. A pH of <2.5, volume of
>0.3ml/kg (20-25ml in average adult) and the
presence of particulate matter result in more
significant lung injury.



James CF, Modell JH, Gibbs CP, Kuck EJ, Ruiz BC. Pulmonary aspiration -- effects of volume and pH in the rat. Anesth Analg 1984;63:665-668
Kennedy TP, Johnson KJ, Kunkel RG, Ward PA, Knight PR, Finch JS. Acute acid aspiration lung injury in the rat: biphasic pathogenesis. Anesth
Analg 1989;69:87-92
Knight PR, Rutter T, Tait AR, Coleman E, Johnson K. Pathogenesis of gastric particulate lung injury: a comparison and
interaction with acidic pneumonitis. Anesth Analg 1993;77:754-760
Aspiration Pneumonitis
Bacteria: under normal circumstances plays no
role in pathogenesis of pneumonitis as gastric
acid prevents growth.
Stomach colonization may occur following use of
antacids, PPIs, and H2 blockers
Gastric Colonization may also occur in patients with
gastroparesis, SBO, and those receiving enteral
feedings.


Spilker CA, Hinthorn DR, Pingleton SK. Intermittent enteral feeding in mechanically ventilated patients: the effect
on gastric pH and gastric cultures. Chest 1996;110:243-248

Aspiration Pneumonia
Aspiration pneumonia: a parenchymal
inflammatory reaction to aspirated material
mediated by an infectious agent, characterized
by an infiltrate on chest radiograph.




McClave SA, DeMeo MT, DeLegge MH et al. North American summit on aspiration in the critical illpatient: consensus
statement. Journal of Parenteral and Enteral Nutrition; 6: S8085.

Aspiration Pneumonia
Pathogens
Polymicrobial in nature
Anaerobic bacteria were initially believed to be a key component
of the aspirate. More recent literature concludes anaerobes play
little role if any. The key microbes are as follows:
Community acquired aspiration pneumonia Streptococcus
pneumoniae, Staphylococcus aureus, H. influenzae
Nosocomial aspiration pneumonia gram negative organisms
including P. aeruginosa



Bartlett JG. Anaerobic infections of the lung. Chest 1987; 91: 69016909
Marik PE, Careau P. The role of anaerobes in patients with ventilator-associated pneumonia and aspiration pneumonia: a
prospective study. Chest 1999;115:178-183
Pneumonitis & Pneumonia
Aspiration
Incidence: difficult to asses due to lack of
sensitive and specific markers. In
addition, most reports are based on
retrospective observational studies of
perioperative database, increasing errors
due to inaccurate documentation.
Incidence & Mortality
Ollson et al
1967-1970 & 1975-1983
Sample size 185,397
Incidence 1/2131 ; Mortality 1/46,340
Warner et al
1985-1991
Sample size 215, 488
Incidence 1/3216 ; Mortality 1/71,829







Olsson GL, Hallen B, Hambraeus-Jonzon K. Aspiration during anaesthesia: a computer-aided study of 185,358 anaesthetics. Acta Anaesthesiol Scand
1986;30:84-92
Warner MA, Warner ME, Weber JG. Clinical significance of pulmonary aspiration during the perioperative period. Anesthesiology 1993;78:56-62
Risk Factors
Stroke neurologic
dysphagia
Disruption of GE junction
Elderly
Pregnant
Diabetes
Renal failure



Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl
J Med. Mar 1 2001;344(9):665-71
Engelhardt T &Webster NR. Pulmonary aspiration of gastric
contents. British Journal of Anaesthesia 1999; 83: 453460

General anesthesia
Emergency
Inadequate anesthesia
Opiods
Difficult airway
Abdominal pathology
Reflux
Signs & Symptoms

Cough
Shortness of breath
Pleuritic chest pain
Tachypnea
Tachycardia
Rales
Decreased breath sounds
Hypoxemia
Fever or hypothermia
Diagnosis
Unless witnessed,
aspiration is a diagnosis
of exclusion based on
history and physical,
laboratory studies +/- new
infiltrate on CXR.




Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J
Med. Mar 1 2001;344(9):665-71
Prevention/Treatment












Practice guidelines for preoperative fasting and the use of pharmacologic agents to reduce the risk of pulmonary aspiration: application to
healthy patients undergoing elective procedures: a report by the American Society of Anesthesiologist Task Force on Preoperative
Fasting. Anesthesiology. 1999 Mar;90(3):896-905
Prevention/Treatment
Antacids, prokinetic agents,
PPIs and H2-blockers have
been shown to decrease
gastric volume and or pH, but
no studies have been shown to
improve outcome.
The ASA does not recommend
the routine administration of
these drugs.




Engelhardt T &Webster NR. Pulmonary aspiration of gastric contents.
British Journal of Anaesthesia 1999; 83: 453460
Practice guidelines for preoperative fasting and the use of pharmacologic
agents to reduce the risk of pulmonary aspiration: application to
healthy patients undergoing elective procedures: a report by the
American Society of Anesthesiologist Task Force on Preoperative
Fasting. Anesthesiology. 1999 Mar;90(3):896-905


Prevention/Treatment
Cricoid Pressure
Described by Sellick in 1961 as a means to prevent
regurgitation and aspiration on induction of anesthesia
by applying backward pressure of the cricoid cartilage
against the bodies of the cervical vertebrae.
Positioning: slight head down tilt, head and neck in full extension
(as in position for tonsillectomy), which increases convexity of
cervical spine and stretches esophagus.



Sellick BA. Cricoid pressure to control regurgitation of stomach contents during induction of anaesthesia. Lancet 1961; 2: 404406.


Prevention/Treatment
Prevention/Treatment
Prevention/Treatment
Cricoid Pressure
Many studies have since been published questioning the
effectiveness and safety of Sellicks maneuver.
Airway obstruction
Diminished view of larynx
Decrease lower esophageal pressure
Esophageal rupture



Brimacombe JR & Berry AM. Cricoid pressure. Canadian Journal of Anaesthesia 1997; 444: 414425
Hartsilver EL & Vanner RG. Airway obstruction with cricoid pressure. Anaesthesia 2000; 55: 208211

Butler J, Sen A. Best evidence topic report. Cricoid pressure in emergency rapid sequence induction. Emerg
Med J. 2005 Nov;22(11):815-6. Review.

Case Report
44 y/o man for emergent appendectomy
Patient was obese with a short neck, but MPC I with TMD 6cm
RSI performed with experienced nurse applying cricoid pressure
DL revealed glottis blocked by overhanging epiglottis
Two attempts at intubation by senior resident unsuccessful. Mask
ventilation with CP difficult.
Patient desaturated. Another attempt to intubate by attending with
CP unsuccessful.
CP then removed and intubation successful.



Ho AM, Wong W, Ling E, Chung DC, Tay BA. Airway difficulties caused by improperly applied cricoid pressure. J
Emerg Med. 2001 Jan;20(1):29-31.
Case Report
81 y/o female in good health with PMHx
disabling rheumatoid arthritis admitted
for investigation of upper abdominal
pain.
Esophagostroscopy revealed large
malignant-appearing gastric ulcer with a
mildly inflamed but otherwise normal
esophagus. Partial gastrectomy
planned
The day prior to surgery she had two
episodes of hematemesis which
required IV resuscitation, including blood
and the decision to operate immediately
was made.
Patient was pre-oxygenated, and RSI
with cricoid pressure was undertaken.

Ralph SJ, Wareham CA. Rupture of the Oesophagus During Cricoid Pressure. Anaesthesia. 1991 Jan;46(1):40-1.
She actively vomited immediately after
12mg etomidate but before loss of
consciousness. Cricoid pressure
discontinued, she was turned to her side
and pharynx aspirated. Sux was given
and she was successfully intubated.
The surgery proceeded and a large
pyloric ulcer was over sewn. The
surgeon also noticed a 10 cm
longitudinal split in the lower esophagus
complete through the wall.
The rupture was repaired and she was
transferred to ICU.
She developed mediastinitis, respiratory
and renal failure and died 10 days after
surgery.
Aspiration Pneumonitis
Treatment
Aggressive suctioning in cases of witnessed aspiration
Routine use of prophylactic antibiotics not recommended unless
SBO
Other conditions associated with gastric colonization
Pneumonitis that fails to resolve within 48 hrs
Corticosteroids not recommended
Intubation if patient is unable to protect airway or in hypoxemia /
respiratory failure



Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med. Mar 1 2001;344(9):665-71
Engelhardt T &Webster NR. Pulmonary aspiration of gastric contents. British Journal of Anaesthesia 1999; 83: 453460


Aspiration Pneumonia
Antibiotic therapy based on setting of
aspiration in addition to characteristics of
patient, eg:
Long term antacid use, SBO, poor dental
hygiene
Antibiotics with anaerobic coverage not
routinely warranted


Marik PE. Aspiration pneumonitis and aspiration pneumonia. N Engl J Med. Mar 1 2001;344(9):665-71


Reflective Practice
The patients NG tube should have been
replaced prior to induction of anesthesia.
As soon as an infiltrate couldnt be ruled
out on CXR the patient should have been
started on appropriate antibiotics
considering she was at high risk of
developing aspiration pneumonia as she
had SBO and was on PPIs for several
days.
Core Competencies
Patient Care
Learned the importance of recognizing the symptoms of aspiration
pneumonia
Medical Knowledge
Reviewed the current literature and recommendations regarding
aspiration pneumonia
Practiced Based Learning and Improvement
Used this case to identify and treat patients at higher risk for aspiration
accordingly.
Interpersonal and Communication Skills
Communicated with attending, patient and nursing staff about patients
condition and further treatment.
Professionalism
Demonstrated respect and compassion for patient.
System Based Practice
Care was coordinated between anesthesia, surgery and ICU teams
References
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453460
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References
Ralph SJ, Wareham CA. Rupture of the Oesophagus During Cricoid Pressure. Anaesthesia. 1991 Jan;46(1):40-1.
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