Infectious Diseases in Critical Care Medicine

CLINICAL APPROACH TO SEVERE CAP BY CXR PATTERN

AND DEGREE OF HYPOXEMIA

Normal hosts with CAP and without significant preexisting cardiopulmonary disease usually

are due to typical pulmonary pathogens and present with segmental/lobar defects with/

without pleural effusion. Pleural effusion is pathogen dependent and is most common with

CAP due to group A streptococci, less commonly withH. influenzae, and very uncommon with

S. pneumoniae.CAP with ill-defined non-segmental/lobar infiltrates usually due to atypical

CAP organisms, i.e., Mycoplasma pneumoniae, which may present as severe CAP in

compromised hosts. Characteristically, Legionella presents radiographically with rapidly

progressive bilateral asymmetric infiltrates. Importantly, it is the behavior of the CXR

infiltrates rather than the location/description of the infiltrates per se, which suggests the

possibility of Legionnaire’s disease (1,8,10).

Excluding Legionnaire’s disease, CAP patients’ bilateral infiltrates, which are primarily

perihilar/interstitial, are not a radiographic feature of the usual typical/atypical CAP

pulmonary pathogens. Bilateral symmetrical/interstitial infiltrates suggest an intracellular

pathogen, e.g., PCP, CMV, influenza A, avian influenza (H5N1), or swine influenza (H1N1)

(Tables 8,9). Excluding CAP mimics, bilateral interstitial infiltrates CAP presenting as severe

CAP are usually due to intracellular pathogens, i.e., viruses or PCP that are associated with

various degrees of hypoxemia. A combination of bilateral perihilar/interstitial infiltrates,

hypoxemia, a;DLCO (carbon monoxide diffusing capacity)/:A–a gradient indicates an

interstitial process, i.e., PCP or viral CAP. There are many noninfectious mimics of CAP that

may present with bilateral infiltrates that are not infectious. In critical care, the common

mimics of CAP in critical care include acute pulmonary edema (due to fluid overload/acute

MI), pulmonary emboli/infarcts, SLE pneumonitis, pulmonary vasculitis, pulmonary drug

reactions, bronchiolitis obliterans organizing pneumonia (BOOP), pulmonary leukostasis,

pulmonary hemorrhage, and acute respiratory distress syndrome (ARDS). With the exception

of viral pneumonias or PCP presenting as severe CAP, bacterial, fungal, or Rickettsial

pneumonias may be accompanied by impressive pulmonary infiltrates but arenotaccompanied

by severe hypoxemia, i.e.,;DLCO/:A–a gradient (>30) (1,8,10) (Tables 10–14).

Severe CAP with Cavitation

Cavitation on the CXR/chest CT scan is an important diagnostic finding in determining the

etiology of severe CAP. Acute cavitary CAPs are severe CAPs because cavitation indicates a

necrotic/hemorrhagic pneumonia. The different diagnosis of severe CAP with cavitation may

be approached clinically by the rapidity of the cavitary process. Cavitation is not a feature of

S. pneumoniaeorH. influenzaeCAP.S. pneumoniaemay be severe with cavitation, which may

Table 8 Swine Influenza (H1N1) Pneumonia: Clinical Case Definitions in Adults{

Definite Swine Influenza (H1N1) Pneumonia (Laboratory Diagnosis)
ILI with temperature of> 1028 F and a CXR with no focal/segmental labor infiltratesplus one or more of these
positive tests:
l Rapid influenza A test
l Respiratory fluorescent antibody (FA) viral panel
l RT-PCR for swine influenza (H1N1)

Probable Swine Influenza (H1N1) Pneumonia (Clinical Diagnosis)
ILI with temperature> 1028 F and a CXR with no focal/segmental labor infiltrateswith negative rapid influenza
diagnostic tests(RIDTs) (see above)*plus this diagnostic triad:
l Severe myalgias
l Otherwise unexplained relative lymphopenia
l Elevated CPK

{During swine influenza (H1N1) pandemic and requiring hospitalization.

*Diagnostic tests negative for other viral CAP pathogens (CMV, SARS, HPS, RSV, metapneumoviruses
parainfluenza viruses, adenoviruses)
Source: Adapted from Ref. 10.

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