injury causing airway edema and unhealed lesions and purulence in the tracheobronchial tree
(Fig. 5). This provides a portal of entry for microbes into the airway and the lung itself. For this
reason, we recommend that pneumonia in the severely burned must be confirmed with the
presence of three conditions, signs of systemic inflammation, radiographic evidence of
pneumonia, and isolation of a pathogen on quantitative culture of a bronchoalveolar lavage
specimen of 10 mL with greater than 10^4 organisms/mL of the return. Those patients with
signs of sepsis and isolation of high colony counts of an organism on bronchoalveolar lavage
without radiographic evidence of pneumonia are considered to have tracheobronchitis, which
can become invasive with subsequent demise. These patients are then documented separately
from those with pneumonia, but are treated similarly with systemic antibiotics directed at the
organism isolated on culture.
Organisms commonly encountered in the tracheobronchial tree include the gram-
negatives, such asPseudomonasandEscherichia coli, and on occasion the gram-positives such as
S. aureus. When the diagnosis of pneumonia or tracheobronchitis is entertained, empiric antibiotic
choice should include one that will cover both these types of organisms. We recommend
imipenem and vancomycin given systemically until the isolates from the bronchoalveolar
lavage are returned. The caveat to this is the finding of gram-negative organisms on routine
surveillance cultures of the wound. Generally, microbes found on the wound do not reliably
predict the causative agent of pneumonia, which requires separate microbial identification. This
is certainly true for gram-positive organisms, but recent data from the U.S. Army Institute of
Surgical Research indicates that identification of gram-negative organisms, particularly
PseudomonasandKlebsiellaon the wound of a patient with pneumonia warrant presumptive
antimicrobial coverage until the causative organism is determined. If sensitivities of the wound
organisms are known, the antimicrobial therapy should at the very least include agents to which
the organisms are sensitive.
Although no such infections have been encountered in our burn patients to date, there is
concern over the recently described necrotizing pneumonias caused by community-acquired
MRSAs producing the Panton–Valentine leukocidin (52). Those organisms can activate
neutrophils within the lung parenchyma, which may then cause rapidly progressing necrosis
associated with a forbiddingly high mortality. Recovery of MRSA, from the bronchus of a
patient with rapidly progressing pneumonia, mandates prompt institution of maximum dose
intravenous vancomycin therapy. The cultured MRSA should be assayed for the leukocidin.
Figure 5 (A) Gross appearance and histology of inhalation injury. Note the denudation and hemorrhagic change
in the trachea wall with erythema and soot. (B) The photomicrograph shows loss of epithelium and soot, which can
lead to tracheobronchitis. Similar inflammatory changes and edema in the distal airway predispose the patient to
pneumonia.
370 Wolf et al.