PULMONARY
PROBLEMS IN THE INFLAMMATION-INFECTION
PHASE
(7
DAYS TO WOUND CLOSURE)
Pulmonary
problems remain a major cause of
morbidity and mortality during this
phase. Pulmonary failure and pulmonary
sepsis exceed burn wound sepsis as a
cause of mortality. There are three
major processes occurring during this
period that will be discussed.
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TABLE
OF CONTENTS
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| 1 |
Nosocomial
Pneumonia
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| 2 |
Hypermetabolism-Induced
Respiratory Fatigue
(Power Failure)
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| 3 |
Adult
Respiratory Distress
Syndrome (Low Pressure
Pulmonary Edema) |
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These
three processes are closely
interrelated. The burn patient is
very prone to infection,
particularly after a
smoke-inhalation injury. The
hypermetabolic state produces a
marked increase in oxygen needs and
carbon dioxide production. The
increased work demands on the lung
as a gas-exchanging organ can exceed
the adequacy of lung function. Adult
respiratory distress syndrome (ARDS)
is a severe complication of the
sepsis process, which is very
difficult to reverse in the burn
patient.
1)
NOSOCOMIAL
PNEUMONIA
Pathophysiology
- Colonization
of the naso-oropharynx
by pathogens
- Aspiration
of infected
tracheobronchial
secretions
- Impairment
of immune defenses
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The
term "nosocomial pneumonia"
refers to the pneumonia that develops
in the hospital with no evidence of
lung infection present on admission,
i.e., it is hospital-acquired.
Although another form of nosocomial
infection, namely, wound infection, is
more common, the mortality rate for
pneumonia is much higher. Burn
patients with a combination of
inhalation injury and a major body
burn have the greatest risk of
pneumonia, with a rate exceeding 50%.
The high incidence is due to the
presence of virulent organisms in the
intensive care unit environment and
the immunosuppressed state of the burn
patient. The major events occurring in
the majority of nosocomial lung
infections are:
Colonization:
Colonization
or bacterial overgrowth of the oro-
and nasopharynx with potential
pathogens occurs in about 50% of
critically burned patients. Nearly
100% of major burn patients with a
major respiratory problem have
colonized their oropharynx with
pathogens. There are a number of
routes and events by which
colonization occurs.
- Transmission
of pathogens on the
hands of hospital
personnel
- Endogenous
organisms from the burn
wound
- Endogenous
organisms colonizing GI
tract via reflux
- Reserves
of pathogens in burn
unit, e.g. respiratory
therapy equipment
- Administration
of broad spectrum
antibiotics
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| Other
Patients Hand Transfer |
| Gastrointestinal
Tract (Aspiration)
----> |
<-----
Burn Wound (Hand Transfer) |
| Change
Normal Flora with
Antibiotics ----> |
<-----
Respiratory Therapy
Equipment |
| Bacterial
Contamination of Lung |
Tracheobronchial
Aspiration:
Aspiration
of infected secretions is the next
step following colonization.
CAUSES
OF TRACHEOBRONCHIAL ASPIRATION
- Pharmacologic
impairment of gag reflex
-
sedation
- paralysis
- Anatomic
impairment to clearance
of secretion
-
oropharnyngeal edema
- endotracheal tube
- nasogastic tube
- Direct
contamination of lower
airways
-
suction catheter
- lavage fluid
- leak around endotracheal
cuff
- increased lung water
- decreased systematic
immune defenses
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Click
to Enlarge
Endotracheal
and oral gastric tube in place
increases make of lower airways
contamination
Impaired
Cough.
Impairment of this reflex is a common
occurrence in the burn patient. A
decrease in the state of consciousness
markedly suppresses both the
initiation of the reflex and the
quality of the cough. This will be the
case with the need for narcotics for
pain control and during recovery from
anesthesia. The ability to take a
large inspiration, necessary for an
adequate cough, will be impaired by a
chest burn and also by muscle weakness
from catabolism. The presence of an
endotracheal tube, although
maintaining an adequate airway, can
decrease the ability to generate a
sufficient propulsive force to clear
secretions effectively. Any aspirated,
infected oral secretions will then
have the opportunity to proliferate.
Impairment
of Containment:
The post burn immunodeficiency
state involving both the cellular
and humoral component of resistance
will impair the ability of the lung
defenses to contain infection. Another
major factor that impairs the
containment process is increasing
lung water. The movement of edema
fluid allows a rapid spread of
bacteria to uninvolved areas both as a
vehicle for carrying bacteria and as
an impairment of the sequestration and
containment process.
DIAGNOSIS
The
early precise diagnoses of the
pneumonia is often very difficult. The
usual criteria for diagnosing
pneumonia are fever, leukocytosis,
purulent sputum, new or increasing
infiltrates on radiographs, and
pathogens growing from the sputum.
These
criteria are of much less value in the
burn patient where other sources of
infection and burn inflammation can
initiate a sepsis syndrome. For
example, approximately 75% of
intensive care unit patients have a
colonized upper airway, usually with
gram-negative organisms. The purulent
sputum may simply be aspirated
oropharyngeal secretions. Pulmonary
infiltrates are also a common finding
in the post burn patient.
Approximately 30% of new infiltrates
in the surgical intensive care unit
patient turn out not to be pneumonia.
Based on these facts, clinical
criteria alone are not sufficiently
accurate to allow a precise diagnosis
of the presence or absence of
nosocomial pneumonia.
Protocol
for Diagnosis of Nosocomial Pneumonia
-
leukocytosis, T° purulent
sputum
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- Proceed
to noninvasive testing
-
quality deep sputum sample
- gram stain of smear
- if not oral secretions,
submit for culture
- chest x-ray, looking for
new infiltrate
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-
Empiric antibiotic
treatment based on smear
and x-ray if immediate
treatment indicated, then
modify according to
culture and response to
therapy OR
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- Initiate
invasive diagnostic
testings if sputum
specimen inadequate or
empiric antibiotics are
a risk of renal
problems. (use of fiber
optic bronchoscopic
assessment and obtaining
of sputum)
-
Treat according to
findings
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