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Distinguishing chemical pneumonitis from bacterial aspiration: still a clinical determination.

Most pneumonia results from microaspiration of bacteria from a previously colonized oropharynx, but some patients develop infection because of macroaspiration of large volumes of gastric or oropharyngeal secretions. When this occurs, it is clinically recognized as an “aspiration syndrome” and is present in patients who have a source of large-volume aspirate (the stomach, often as a result of recent eating or abnormal motility) in the setting of impaired oropharyngeal reflexes, usually as the result of a reduced level of consciousness or as a consequence of neurologic illness (1). When macroaspiration occurs, it can lead to several types of pulmonary injury, which are difficult to distinguish from one another on clinical grounds, with some needing antibiotic therapy and others not. These include aspiration of gastric acid leading to a chemical pneumonitis or aspiration of bacteria leading to infectious pneumonia. In addition, patients can aspirate food material or foreign bodies, which can obstruct the airway and predispose to distal pneumonia, and they can develop secondary bacterial pneumonia that superinfects a lung that has been injured by gastric acid. As a clinician, it is challenging to decide when to start antibiotic therapy in a patient with an aspiration syndrome, because all of these patients can have lung infiltrates, but antibiotics are only beneficial for pneumonia and not for chemical pneumonitis. In the current issue of Critical Care Medicine, El Solh and colleagues (2), who have done some of the most elegant research in this area, have attempted to determine whether the use of a serum biomarker, procalcitonin (PCT), could be used to separate chemical pneumonitis from bacterial pneumonia in patients with aspiration syndrome. They enrolled 65 consecutive patients with pulmonary aspiration, all of whom were intubated and mechanically ventilated and all having lung infiltrates and measured serum PCT on day 1 and day 3 and collected bronchoalveolar lavage for quantitative cultures within 6 hrs of initial intubation. All patients had aspiration risk factors, including neurodegenerative disease (n 24), drug overdose (n 15), cerebrovascular accident (n 14), or seizure (n 11). Using a 10-colony-forming unit/mL cutoff, 32 patients had bacterial pneumonia, but there was no correlation between the presence of bacterial pneumonia and PCT levels in contrast to studies in other populations of pneumonia patients, in which PCT could separate patients with lung infiltrates as a result of bacterial infection from those with a nonbacterial cause of lung infiltrates (3). Interestingly, in both populations, PCT levels were elevated compared with a control population without pneumonia, suggesting that all patients had a high level of inflammation present. When patients had PCT levels on day 3 that were lower than on day 1, there was a shorter duration of both mechanical ventilation and antibiotic therapy and a lower likelihood of dying than if PCT levels did not fall. The study demonstrated that PCT was not useful, when measured on admission in patients with aspiration syndrome, in predicting whether bacterial pneumonia was present and thus could not be used to guide the decision about whether such a patient with lung infiltrates would benefit from antibiotic therapy. It is also interesting to consider the bacteriology of aspiration pneumonia in intensive care unit patients that was found in this and in other studies. In a previous study of 95 residents of longterm care facilities who had severe aspiration pneumonia treated with mechanical ventilation, bacteriologic data were collected by performing protected bronchoalveolar lavage within 4 hrs of admission (4). Gram-negative enteric bacilli were present in 49%, Staphylococcus aureus was in 12%, whereas only 16% had anaerobes present and when present, they were often with aerobic bacteria and patients usually recovered without receiving specific antianaerobic therapy. In the current study, which did not include only those residing in nursing homes, the bacteriology was slightly different, with S. aureus and Escherichia coli being the most common organisms identified but with anaerobes present in 10 of 36 bacterial isolates from 32 patients. The findings from these two studies make it very clear that even when infection, and not chemical pneumonitis, is present, routine anaerobic therapy is not needed in most patients with aspiration pneumonia and that this therapy is rarely, if ever, needed in nursing home residents with severe aspiration pneumonia. It is important for intensive care unit doctors to be aware of these findings given the possibility that antianaerobic therapy can lead to the emergence of both Clostridium difficile and vancomycin-resistant Enterococcus, and thus it is possible to avoid the gratuitous use of these agents in most patients with aspiration syndrome. The findings in the current study by El Solh and colleagues indicate that the decision to start antibiotic therapy should be a clinical one and not one based on the measurement of biomarkers. In many ways, these findings are not surprising. An older study of 23 patients with closed head injury found that those with aspiration had a higher PCT level than those without aspiration, and that nonsurvivors had higher PCT values than survivors (5). However, in that study, in contrast to the study by El Solh et al, not all patients had aspiration or lung infiltrates, and there was no effort made to separate chemical from bacterial aspiration syndromes. In both of these studies, it seems that when *See also p. 1251.