Ventilator-associated pneumonia


Ventilator-associated pneumonia is a
type of lung infection that occurs in people who are on breathing machines in
hospitals. As such, VAP typically affects critically ill persons that are
in an intensive care unit. VAP is a major source of increased illness, and
death. Persons with VAP have increased lengths of ICU hospitalization and have
up to a 20-30% death rate. The diagnosis of VAP varies among hospitals and
providers but usually requires a new infiltrate on chest x-ray plus two or
more other factors. These factors include temperature of>38 °C or 12 ×
109/ml, purulent secretions from the airways in the lung, and/or reduction in
gas exchange. Signs and symptoms
People who are on mechanical ventilation are often sedated and are rarely able to
communicate. As such, many of the typical symptoms of pneumonia will
either be absent or unable to be obtained. The most important signs are
fever or low body temperature, new purulent sputum, and hypoxemia.
Cause =Risk factors=
Risk factors for VAP include underlying heart or lung disease, neurologic
disease, and trauma, as well as modifiable risk factors such as whether
the head of the bed is flat or raised, whether the patient had an aspiration
event before intubation, and prior antibiotic exposure. Patients who are in
the ICU for head trauma or other severe neurologic illness, as well as patients
who are in the ICU for blunt or penetrating trauma, are at especially
high risk of developing VAP. Further, patients hospitalized for blunt trauma
are at a higher risk of developing VAP compared to patients with penetrating
trauma.=Microbiology=
The microbiologic flora responsible for VAP is different from that of the more
common community-acquired pneumonia. In particular, viruses and fungi are
uncommon causes in people who do not have underlying immune deficiencies.
Though any microorganism that causes CAP can cause VAP, there are several
bacteria which are particularly important causes of VAP because of their
resistance to commonly used antibiotics. These bacteria are referred to as
multidrug resistant. Pseudomonas aeruginosa is the most
common MDR Gram-negative bacterium causing VAP. Pseudomonas has natural
resistance to many antibiotics and has been known to acquire resistance to
every antibiotic except for polymyxin B. Resistance is typically acquired through
upregulation or mutation of a variety of efflux pumps which pump antbiotics out
of the cell. Resistance may also occur through loss of an outer membrane porin
channel Klebsiella pneumoniae has natural
resistance to some beta-lactam antibiotics such as ampicillin.
Resistance to cephalosporins and aztreonam may arise through induction of
a plasmid-based extended spectrum beta-lactamase or plasmid-based
ampC-type enzyme Serratia marcescens has an ampC gene
which can be induced by exposure to antibiotics such as cephalosporins.
Thus, culture sensitivities may initially indicate appropriate treatment
which fails due to bacterial response. Enterobacter as a group also have an
inducible ampC gene. Enterobacter may also develop resistance by acquiring
plasmids. Citrobacter also has an inducible ampC
gene. Stenotrophomonas maltophilia often
colonizes people who have tracheal tubes but can also cause pneumonia. It is
often resistant to a wide array of antibiotics but is usually sensitive to
co-trimoxazole Acinetobacter are becoming more common
and may be resistant to carbapenems such as imipenem and meropenem
Burkholderia cepacia is an important organism in people with cystic fibrosis
and is often resistant to multiple antibiotics
Methicillin-resistant Staphylococcus aureus is an increasing cause of VAP. As
many as fifty percent of Staphylococcus aureus isolates in the intensive care
setting are resistant to methicillin. Resistance is conferred by the mecA
gene. Pathophysiology
It is thought by many, that VAP primarily occurs because the
endotracheal or tracheostomy tube allows free passage of bacteria into the lower
segments of the lung in a person who often has underlying lung or immune
problems. Bacteria travel in small droplets both through the endotracheal
tube and around the cuff. Often, bacteria colonize the endotracheal or
tracheostomy tube and are embolized into the lungs with each breath. Bacteria may
also be brought down into the lungs with procedures such as deep suctioning or
bronchoscopy. Another possibility is that the bacteria already exist in the
mucus lining the bronchial tree, and are just kept in check by the body’s first
line of defenses. Ciliary action of the cells lining the trachea drive the mucus
superiorly, leading to a build-up of fluids around the inflated cuff where
there is little to no airway clearance. The bacteria can then colonize easily
without disturbance and then rise in numbers enough to become infective. The
droplets that are driven into the airstream and into the lung fields are
lofted by way of Bernoulli’s principle. There is also a condition called
oxidative damage that occurs when concentrations of pure oxygen come into
prolonged contact with cells and this damages the cilia of the cells, thus
inhibiting their action as part of the body’s first line of defense.
Whether bacteria also travel from the sinuses or the stomach into the lungs
is, as of 2005, controversial. However, spread to the lungs from the blood
stream or the gut is uncommon. Once inside the lungs, bacteria then
take advantage of any deficiencies in the immune system and multiply. A
combination of bacterial damage and consequences of the immune response lead
to disruption of gas exchange with resulting symptoms.
Diagnosis Diagnosis of ventilator-associated
pneumonia is difficult and is not standardized. The criteria used for
diagnosis of VAP varies by institution, but tends to be a combination of several
of the following radiographic, clinical sign, and laboratory evidence:
Temperature greater than 38C or less than 36C
White blood cell count greater than 12,000/mm3 or less than 4,000/mm3
Purulent secretions, increased secretions, or change in secretions
Positive tracheal cultures or bronchoalvelolar lavage cultures
Some sign of respiratory distress, such as shortness of breath, rapid breathing,
abnormal breathing sounds when listening with stethoscope
Increased need for oxygen on the ventilator
Chest X-Rays: at least two serial xrays showing sustained or worsening shadowing
Positive cultures that were obtained directly from the lung environment, such
as from the trachea or bronchioles As an example, some institutions may
require one clinical symptoms such as shortness of breath, one clinical sign
such as fever, plus evidence on chest xray and in tracheal cultures.
There is no gold standard for getting cultures or other evidence of bacterial,
viral, or fungal culprit. One strategy collects cultures from the trachea of
people with symptoms of VAP. Another is more invasive and advocates a
bronchoscopy plus bronchoalveolar lavage for people with symptoms of VAP. Both
strategies also require a new or enlarging infiltrate on chest x-ray as
well as clinical signs/symptoms such as fever and shortness of breath.
Blood cultures may reveal the microorganisms causing VAP, but are
often not helpful as they are positive in only 25% of clinical VAP cases. Even
in cases with positive blood cultures, the bacteremia may be from a source
other than the lung infection. Prevention
Prevention of VAP involves limiting exposure to resistant bacteria,
discontinuing mechanical ventilation as soon as possible, and a variety of
strategies to limit infection while intubated. Resistant bacteria are spread
in much the same ways as any communicable disease. Proper hand
washing, sterile technique for invasive procedures, and isolation of individuals
with known resistant organisms are all mandatory for effective infection
control. A variety of aggressive weaning protocols to limit the amount of time a
person spends intubated have been proposed. One important aspect is
limiting the amount of sedation that a ventilated person receives.
Other recommendations for preventing VAP include raising the head of the bed to
at least 30 degrees. Antiseptic mouthwashes such as chlorhexidine may
also reduce the incidence of VAP, although the evidence is mainly
restricted to those who have undergone cardiac surgery.
American and Canadian guidelines strongly recommend the use of
supraglottic secretion drainage Special tracheal tubes with an incorporated
suction lumen as the EVAC tracheal tube form Covidien / Mallinckrodt can be used
for that reason. New cuff technology based on polyurethane material in
combination with subglottic drainageshowed significant delay in
early and late onset of VAP. A recent clinical trial indicates that
the use of silver-coated endotracheal tubes may also reduce the incidence of
VAP. There is tentative evidence that the use of probiotics may reduced the
likelihood of getting VAP, however it is unclear if probiotics have an impact on
ICU or in-hospital death. Treatment
Treatment of VAP should be matched to known causative bacteria. However, when
VAP is first suspected, the bacteria causing infection is typically not known
and broad-spectrum antibiotics are given until the particular bacterium and its
sensitivities are determined. Empiric antibiotics should take into account
both the risk factors a particular individual has for resistant bacteria as
well as the local prevalence of resistant microorganisms. If a person
has previously had episodes of pneumonia, information may be available
about prior causative bacteria. The choice of initial therapy is therefore
entirely dependent on knowledge of local flora and will vary from hospital to
hospital. Risk factors for infection with an MDR
strain include ventilation for more than five days, recent hospitalization,
residence in a nursing home, treatment in a hemodialysis clinic, and prior
antibiotic use. Possible empirical therapy combinations
include: vancomycin/linezolid and ciprofloxacin,
cefepime and gentamicintobramycin vancomycin/linezolid and ceftazidime
Ureidopenicillin plus β-lactamase inhibitor such as
piperacillin/tazobactam or ticarcillin/clavulanate
a carbapenem Therapy is typically changed once the
causative bacteria are known and continued until symptoms resolve. For
patients with VAP not caused by nonfermenting Gram-negative bacilli the
available evidence seems to support the use of short-course antimicrobial
treatments (

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